<?xml version="1.0" encoding="UTF-8"?>
<rss version="2.0">
    <channel>
        <title>Neural Plasticity via MedWorm.com</title>
        <description>MedWorm.com provides a medical RSS filtering service. Over 6000 RSS medical sources are combined and output via different filters. This feed contains the latest items from the 'Neural Plasticity' source.</description>
        <link><![CDATA[http://www.medworm.com/rss/search.php?qu=Neural+Plasticity&t=Neural+Plasticity&s=Search&f=source]]></link>
        <lastBuildDate>Wed, 08 Feb 2012 20:43:26 +0100</lastBuildDate>
        <item>
            <title>Modulation of CREB in the Dorsal Lateral Geniculate Nucleus of Dark-Reared Mice.</title>
            <link>http://www.medworm.com/index.php?rid=5664344&amp;cid=s_36794_25_f&amp;fid=36794&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22292123%26dopt%3DAbstract</link>
            <description>Authors: Krahe TE, Seabrook TA, Chen CK, Fox MA, Guido W
    Abstract
    The cAMP-response element-binding protein (CREB) plays an important role in visual cortical plasticity that follows the disruption of sensory activity, as induced by dark rearing (DR). Recent findings indicate that the dorsal lateral geniculate nucleus (dLGN) of thalamus is also sensitive to altered sensory activity. DR disrupts retinogeniculate synaptic strength and pruning in mice, but only when DR starts one week after eye opening (delayed DR, DDR) and not after chronic DR (CDR) from birth. While DR upregulates CREB in visual cortex, whether it also modulates this pathway in dLGN remains unknown. Here we investigate the role of CREB in the dLGN of mice that were CDR or DDR using western blot and immunofluorescence...</description>
            <author>Neural Plasticity</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5664344</comments>
            <pubDate>Mon, 06 Feb 2012 22:24:02 +0100</pubDate>
            <guid isPermaLink="false">5664344</guid>        </item>
        <item>
            <title>From Spinal Central Pattern Generators to Cortical Network: Integrated BCI for Walking Rehabilitation.</title>
            <link>http://www.medworm.com/index.php?rid=5627472&amp;cid=s_36794_25_f&amp;fid=36794&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22272380%26dopt%3DAbstract</link>
            <description>Authors: Cheron G, Duvinage M, De Saedeleer C, Castermans T, Bengoetxea A, Petieau M, Seetharaman K, Hoellinger T, Dan B, Dutoit T, Sylos Labini F, Lacquaniti F, Ivanenko Y
    Abstract
    Success in locomotor rehabilitation programs can be improved with the use of brain-computer interfaces (BCIs). Although a wealth of research has demonstrated that locomotion is largely controlled by spinal mechanisms, the brain is of utmost importance in monitoring locomotor patterns and therefore contains information regarding central pattern generation functioning. In addition, there is also a tight coordination between the upper and lower limbs, which can also be useful in controlling locomotion. The current paper critically investigates different approaches that are applicable to this field: the use...</description>
            <author>Neural Plasticity</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5627472</comments>
            <pubDate>Thu, 26 Jan 2012 02:12:03 +0100</pubDate>
            <guid isPermaLink="false">5627472</guid>        </item>
        <item>
            <title>Spines, plasticity, and cognition in Alzheimer's model mice.</title>
            <link>http://www.medworm.com/index.php?rid=5553239&amp;cid=s_36794_25_f&amp;fid=36794&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22203915%26dopt%3DAbstract</link>
            <description>Authors: Spires-Jones T, Knafo S
    Abstract
    The pathological hallmarks of Alzheimer's disease (AD)-widespread synaptic and neuronal loss and the pathological accumulation of amyloid-beta peptide (Aβ) in senile plaques, as well as hyperphosphorylated tau in neurofibrillary tangles-have been known for many decades, but the links between AD pathology and dementia and effective therapeutic strategies remain elusive. Transgenic mice have been developed based on rare familial forms of AD and frontotemporal dementia, allowing investigators to test in detail the structural, functional, and behavioral consequences of AD-associated pathology. Here, we review work on transgenic AD models that investigate the degeneration of dendritic spine structure, synaptic function, and cognition. Together,...</description>
            <author>Neural Plasticity</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5553239</comments>
            <pubDate>Sat, 31 Dec 2011 22:24:18 +0100</pubDate>
            <guid isPermaLink="false">5553239</guid>        </item>
        <item>
            <title>Selective estrogen receptor modulators regulate dendritic spine plasticity in the hippocampus of male rats.</title>
            <link>http://www.medworm.com/index.php?rid=5539616&amp;cid=s_36794_25_f&amp;fid=36794&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22164341%26dopt%3DAbstract</link>
            <description>In this study, we have explored whether raloxifene and tamoxifen may regulate the number and geometry of dendritic spines in CA1 pyramidal neurons of the rat hippocampus. Young adult male rats were injected with raloxifene (1 mg/kg), tamoxifen (1 mg/kg), or vehicle and killed 24 h after the injection. Animals treated with raloxifene or tamoxifen showed an increased numerical density of dendritic spines in CA1 pyramidal neurons compared to animals treated with vehicle. Raloxifene and tamoxifen had also specific effects in the morphology of spines. These findings suggest that raloxifene and tamoxifen may influence the processing of information by hippocampal pyramidal neurons by affecting the number and shape of dendritic spines.
    PMID: 22164341 [PubMed - in process] (Source: Neural...</description>
            <author>Neural Plasticity</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5539616</comments>
            <pubDate>Sun, 25 Dec 2011 16:48:11 +0100</pubDate>
            <guid isPermaLink="false">5539616</guid>        </item>
        <item>
            <title>Place cells, grid cells, attractors, and remapping.</title>
            <link>http://www.medworm.com/index.php?rid=5481626&amp;cid=s_36794_25_f&amp;fid=36794&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22135756%26dopt%3DAbstract</link>
            <description>Authors: Jeffery KJ
    Abstract
    Place and grid cells are thought to use a mixture of external sensory information and internal attractor dynamics to organize their activity. Attractor dynamics may explain both why neurons react coherently following sufficiently large changes to the environment (discrete attractors) and how firing patterns move smoothly from one representation to the next as an animal moves through space (continuous attractors). However, some features of place cell behavior, such as the sometimes independent responsiveness of place cells to environmental change (called &quot;remapping&quot;), seem hard to reconcile with attractor dynamics. This paper suggests that the explanation may be found in an anatomical separation of the two attractor systems coupled with a dynamic context...</description>
            <author>Neural Plasticity</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5481626</comments>
            <pubDate>Thu, 08 Dec 2011 03:06:02 +0100</pubDate>
            <guid isPermaLink="false">5481626</guid>        </item>
        <item>
            <title>Deafferentation-Induced Redistribution of MMP-2, but Not of MMP-9, Depends on the Emergence of GAP-43 Positive Axons in the Adult Rat Cochlear Nucleus.</title>
            <link>http://www.medworm.com/index.php?rid=5481625&amp;cid=s_36794_25_f&amp;fid=36794&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22135757%26dopt%3DAbstract</link>
            <description>In conclusion, GAP-43-containing axons emerging in AVCN after cochlear ablation seem to be causal for the maintenance of MMP-2-mediated ECM remodeling.
    PMID: 22135757 [PubMed - in process] (Source: Neural Plasticity)</description>
            <author>Neural Plasticity</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5481625</comments>
            <pubDate>Thu, 08 Dec 2011 03:06:02 +0100</pubDate>
            <guid isPermaLink="false">5481625</guid>        </item>
        <item>
            <title>Cortical Plasticity during Motor Learning and Recovery after Ischemic Stroke.</title>
            <link>http://www.medworm.com/index.php?rid=5481624&amp;cid=s_36794_25_f&amp;fid=36794&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22135758%26dopt%3DAbstract</link>
            <description>Authors: Hosp JA, Luft AR
    Abstract
    The motor system has the ability to adapt to environmental constraints and injury to itself. This adaptation is often referred to as a form of plasticity allowing for livelong acquisition of new movements and for recovery after stroke. We are not sure whether learning and recovery work via same or similar neural mechanisms. But, all these processes require widespread changes within the matrix of the brain. Here, basic mechanisms of these adaptations on the level of cortical circuitry and networks are reviewed. We focus on the motor cortices because their role in learning and recovery has been investigated more thoroughly than other brain regions.
    PMID: 22135758 [PubMed - in process] (Source: Neural Plasticity)</description>
            <author>Neural Plasticity</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5481624</comments>
            <pubDate>Thu, 08 Dec 2011 03:06:02 +0100</pubDate>
            <guid isPermaLink="false">5481624</guid>        </item>
        <item>
            <title>A Neural Correlate of Predicted and Actual Reward-Value Information in Monkey Pedunculopontine Tegmental and Dorsal Raphe Nucleus during Saccade Tasks.</title>
            <link>http://www.medworm.com/index.php?rid=5383703&amp;cid=s_36794_25_f&amp;fid=36794&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22013541%26dopt%3DAbstract</link>
            <description>Authors: Okada K, Nakamura K, Kobayashi Y
    Abstract
    Dopamine, acetylcholine, and serotonin, the main modulators of the central nervous system, have been proposed to play important roles in the execution of movement, control of several forms of attentional behavior, and reinforcement learning. While the response pattern of midbrain dopaminergic neurons and its specific role in reinforcement learning have been revealed, the role of the other neuromodulators remains rather elusive. Here, we review our recent studies using extracellular recording from neurons in the pedunculopontine tegmental nucleus, where many cholinergic neurons exist, and the dorsal raphe nucleus, where many serotonergic neurons exist, while monkeys performed eye movement tasks to obtain different reward values. The...</description>
            <author>Neural Plasticity</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5383703</comments>
            <pubDate>Tue, 08 Nov 2011 13:55:02 +0100</pubDate>
            <guid isPermaLink="false">5383703</guid>        </item>
        <item>
            <title>GABAergic circuit development and its implication for CNS disorders.</title>
            <link>http://www.medworm.com/index.php?rid=5383702&amp;cid=s_36794_25_f&amp;fid=36794&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22013542%26dopt%3DAbstract</link>
            <description>Authors: Di Cristo G, Pizzorusso T, Cancedda L, Sernagor E
    PMID: 22013542 [PubMed - in process] (Source: Neural Plasticity)</description>
            <author>Neural Plasticity</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5383702</comments>
            <pubDate>Tue, 08 Nov 2011 13:55:02 +0100</pubDate>
            <guid isPermaLink="false">5383702</guid>        </item>
        <item>
            <title>Motor cortical networks for skilled movements have dynamic properties that are related to accurate reaching.</title>
            <link>http://www.medworm.com/index.php?rid=5333283&amp;cid=s_36794_25_f&amp;fid=36794&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22007332%26dopt%3DAbstract</link>
            <description>Authors: Putrino DF, Chen Z, Ghosh S, Brown EN
    Abstract
    Neurons in the Primary Motor Cortex (MI) are known to form functional ensembles with one another in order to produce voluntary movement. Neural network changes during skill learning are thought to be involved in improved fluency and accuracy of motor tasks. Unforced errors during skilled tasks provide an avenue to study network connections related to motor learning. In order to investigate network activity in MI, microwires were implanted in the MI of cats trained to perform a reaching task. Spike trains from eight groups of simultaneously recorded cells (95 neurons in total) were acquired. A point process generalized linear model (GLM) was developed to assess simultaneously recorded cells for functional connectivity during re...</description>
            <author>Neural Plasticity</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5333283</comments>
            <pubDate>Fri, 21 Oct 2011 07:50:02 +0100</pubDate>
            <guid isPermaLink="false">5333283</guid>        </item>
        <item>
            <title>Neuroplasticity of the Sensorimotor Cortex during Learning.</title>
            <link>http://www.medworm.com/index.php?rid=5284477&amp;cid=s_36794_25_f&amp;fid=36794&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21949908%26dopt%3DAbstract</link>
            <description>Authors: Francis JT, Song W
    Abstract
    We will discuss some of the current issues in understanding plasticity in the sensorimotor (SM) cortices on the behavioral, neurophysiological, and synaptic levels. We will focus our paper on reaching and grasping movements in the rat. In addition, we will discuss our preliminary work utilizing inhibition of protein kinase Mζ (PKMζ), which has recently been shown necessary and sufficient for the maintenance of long-term potentiation (LTP) (Ling et al., 2002). With this new knowledge and inhibitors to this system, as well as the ability to overexpress this system, we can start to directly modulate LTP and determine its influence on behavior as well as network level processing dependent at least in part due to this form of LTP. We will also brie...</description>
            <author>Neural Plasticity</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5284477</comments>
            <pubDate>Wed, 05 Oct 2011 19:00:02 +0100</pubDate>
            <guid isPermaLink="false">5284477</guid>        </item>
        <item>
            <title>Associative memory storage and retrieval: involvement of theta oscillations in hippocampal information processing.</title>
            <link>http://www.medworm.com/index.php?rid=5284476&amp;cid=s_36794_25_f&amp;fid=36794&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21961072%26dopt%3DAbstract</link>
            <description>Authors: Stella F, Treves A
    Abstract
    Theta oscillations are thought to play a critical role in neuronal information processing, especially in the hippocampal region, where their presence is particularly salient. A detailed description of theta dynamics in this region has revealed not only a consortium of layer-specific theta dipoles, but also within-layer differences in the expression of theta. This complex and articulated arrangement of current flows is reflected in the way neuronal firing is modulated in time. Several models have proposed that these different theta modulators flexibly coordinate hippocampal regions, to support associative memory formation and retrieval. Here, we summarily review different approaches related to this issue and we describe a mechanism, based on expe...</description>
            <author>Neural Plasticity</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5284476</comments>
            <pubDate>Wed, 05 Oct 2011 19:00:02 +0100</pubDate>
            <guid isPermaLink="false">5284476</guid>        </item>
        <item>
            <title>Ripples make waves: binding structured activity and plasticity in hippocampal networks.</title>
            <link>http://www.medworm.com/index.php?rid=5284475&amp;cid=s_36794_25_f&amp;fid=36794&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21961073%26dopt%3DAbstract</link>
            <description>Authors: Sadowski JH, Jones MW, Mellor JR
    Abstract
    Establishing novel episodic memories and stable spatial representations depends on an exquisitely choreographed, multistage process involving the online encoding and offline consolidation of sensory information, a process that is largely dependent on the hippocampus. Each step is influenced by distinct neural network states that influence the pattern of activation across cellular assemblies. In recent years, the occurrence of hippocampal sharp wave ripple (SWR) oscillations has emerged as a potentially vital network phenomenon mediating the steps between encoding and consolidation, both at a cellular and network level by promoting the rapid replay and reactivation of recent activity patterns. Such events facilitate memory formation...</description>
            <author>Neural Plasticity</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5284475</comments>
            <pubDate>Wed, 05 Oct 2011 19:00:02 +0100</pubDate>
            <guid isPermaLink="false">5284475</guid>        </item>
        <item>
            <title>Presynaptic Ionotropic Receptors Controlling and Modulating the Rules for Spike Timing-Dependent Plasticity.</title>
            <link>http://www.medworm.com/index.php?rid=5249824&amp;cid=s_36794_25_f&amp;fid=36794&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21941664%26dopt%3DAbstract</link>
            <description>Authors: Verhoog MB, Mansvelder HD
    Abstract
    Throughout life, activity-dependent changes in neuronal connection strength enable the brain to refine neural circuits and learn based on experience. In line with predictions made by Hebb, synapse strength can be modified depending on the millisecond timing of action potential firing (STDP). The sign of synaptic plasticity depends on the spike order of presynaptic and postsynaptic neurons. Ionotropic neurotransmitter receptors, such as NMDA receptors and nicotinic acetylcholine receptors, are intimately involved in setting the rules for synaptic strengthening and weakening. In addition, timing rules for STDP within synapses are not fixed. They can be altered by activation of ionotropic receptors located at, or close to, synapses. Here, we...</description>
            <author>Neural Plasticity</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5249824</comments>
            <pubDate>Sun, 25 Sep 2011 02:04:02 +0100</pubDate>
            <guid isPermaLink="false">5249824</guid>        </item>
        <item>
            <title>Reactivation, replay, and preplay: how it might all fit together.</title>
            <link>http://www.medworm.com/index.php?rid=5235460&amp;cid=s_36794_25_f&amp;fid=36794&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21918724%26dopt%3DAbstract</link>
            <description>Authors: Buhry L, Azizi AH, Cheng S
    Abstract
    Sequential activation of neurons that occurs during &quot;offline&quot; states, such as sleep or awake rest, is correlated with neural sequences recorded during preceding exploration phases. This so-called reactivation, or replay, has been observed in a number of different brain regions such as the striatum, prefrontal cortex, primary visual cortex and, most prominently, the hippocampus. Reactivation largely co-occurs together with hippocampal sharp-waves/ripples, brief high-frequency bursts in the local field potential. Here, we first review the mounting evidence for the hypothesis that reactivation is the neural mechanism for memory consolidation during sleep. We then discuss recent results that suggest that offline sequential activity in the wa...</description>
            <author>Neural Plasticity</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5235460</comments>
            <pubDate>Tue, 20 Sep 2011 21:08:02 +0100</pubDate>
            <guid isPermaLink="false">5235460</guid>        </item>
        <item>
            <title>GABA Neuron Alterations, Cortical Circuit Dysfunction and Cognitive Deficits in Schizophrenia.</title>
            <link>http://www.medworm.com/index.php?rid=5221891&amp;cid=s_36794_25_f&amp;fid=36794&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21904685%26dopt%3DAbstract</link>
            <description>Authors: Gonzalez-Burgos G, Fish KN, Lewis DA
    Abstract
    Schizophrenia is a brain disorder associated with cognitive deficits that severely affect the patients' capacity for daily functioning. Whereas our understanding of its pathophysiology is limited, postmortem studies suggest that schizophrenia is associated with deficits of GABA-mediated synaptic transmission. A major role of GABA-mediated transmission may be producing synchronized network oscillations which are currently hypothesized to be essential for normal cognitive function. Therefore, cognitive deficits in schizophrenia may result from a GABA synapse dysfunction that disturbs neural synchrony. Here, we highlight recent studies further suggesting alterations of GABA transmission and network oscillations in schizophrenia. W...</description>
            <author>Neural Plasticity</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5221891</comments>
            <pubDate>Fri, 16 Sep 2011 04:32:02 +0100</pubDate>
            <guid isPermaLink="false">5221891</guid>        </item>
        <item>
            <title>Interplay of amygdala and cingulate plasticity in emotional fear.</title>
            <link>http://www.medworm.com/index.php?rid=5221890&amp;cid=s_36794_25_f&amp;fid=36794&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21912749%26dopt%3DAbstract</link>
            <description>Authors: Toyoda H, Li XY, Wu LJ, Zhao MG, Descalzi G, Chen T, Koga K, Zhuo M
    Abstract
    The amygdala is known to be a critical brain region for emotional fear. It is believed that synaptic plasticity within the amygdala is the cellular basis of fear memory. Recent studies demonstrate that cortical areas such as the prefrontal cortex (PFC) and anterior cingulate cortex (ACC) may also contribute to the formation of fear memory, including trace fear memory and remote fear memory. At synaptic level, fear conditioning also triggers plastic changes within the cortical areas immediately after the condition. These results raise the possibility that certain forms of synaptic plasticity may occur within the cortex while synaptic potentiation takes place within synapses in the hippocampus and a...</description>
            <author>Neural Plasticity</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5221890</comments>
            <pubDate>Fri, 16 Sep 2011 04:32:02 +0100</pubDate>
            <guid isPermaLink="false">5221890</guid>        </item>
        <item>
            <title>Synthesis and Characterization of Sb2S3 Nanorods via Complex Decomposition Approach</title>
            <link>http://www.medworm.com/index.php?rid=5220639&amp;cid=s_36794_168_f&amp;fid=37050&amp;url=http%3A%2F%2Fwww.hindawi.com%2Fjournals%2Fjnm%2F2011%2F414798%2F</link>
            <description>Based on the complex decomposition approach, a simple hydrothermal method has been developed for the synthesizing of Sb2S3 nanorods with high yield in 24&amp;#x2009;h at 150&amp;#x2218;C. The powder X-ray diffraction pattern shows the Sb2S3 crystals belong to the orthorhombic phase with calculated lattice parameters a=1.120&amp;#x2009;nm, b=1.128&amp;#x2009;nm, and c=0.383&amp;#x2009;nm. The quantification of energy dispersive X-ray spectrometric analysis peaks give an atomic ratio of 2&amp;#x2009;:&amp;#x2009;3 for Sb&amp;#x2009;:&amp;#x2009;S. TEM and SEM studies reveal that the appearance of the as-prepared Sb2S3 is rod-like which is composed of nanorods with the typical width of 30&amp;#8211;160&amp;#x2009;nm and length of up to 6&amp;#x2009;&amp;#x003bc;m. High-resolution transmission electron microscopic (HRTEM) studies reveal that th...</description>
            <author>Neural Plasticity</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5220639</comments>
            <pubDate>Thu, 15 Sep 2011 15:32:39 +0100</pubDate>
            <guid isPermaLink="false">5220639</guid>        </item>
        <item>
            <title>Histaminergic mechanisms for modulation of memory systems.</title>
            <link>http://www.medworm.com/index.php?rid=5180525&amp;cid=s_36794_25_f&amp;fid=36794&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21876818%26dopt%3DAbstract</link>
            <description>Authors: Köhler CA, da Silva WC, Benetti F, Bonini JS
    Abstract
    Encoding for several memory types requires neural changes and the activity of distinct regions across the brain. These areas receive broad projections originating in nuclei located in the brainstem which are capable of modulating the activity of a particular area. The histaminergic system is one of the major modulatory systems, and it regulates basic homeostatic and higher functions including arousal, circadian, and feeding rhythms, and cognition. There is now evidence that histamine can modulate learning in different types of behavioral tasks, but the exact course of modulation and its mechanisms are controversial. In the present paper we review the involvement of the histaminergic system and the effects histaminergic...</description>
            <author>Neural Plasticity</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5180525</comments>
            <pubDate>Fri, 02 Sep 2011 04:44:02 +0100</pubDate>
            <guid isPermaLink="false">5180525</guid>        </item>
        <item>
            <title>Mechanisms of GABAergic homeostatic plasticity.</title>
            <link>http://www.medworm.com/index.php?rid=5180524&amp;cid=s_36794_25_f&amp;fid=36794&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21876819%26dopt%3DAbstract</link>
            <description>Authors: Wenner P
    Abstract
    Homeostatic plasticity ensures that appropriate levels of activity are maintained through compensatory adjustments in synaptic strength and cellular excitability. For instance, excitatory glutamatergic synapses are strengthened following activity blockade and weakened following increases in spiking activity. This form of plasticity has been described in a wide array of networks at several different stages of development, but most work and reviews have focussed on the excitatory inputs of excitatory neurons. Here we review homeostatic plasticity of GABAergic neurons and their synaptic connections. We propose a simplistic model for homeostatic plasticity of GABAergic components of the circuitry (GABAergic synapses onto excitatory neurons, excitatory connect...</description>
            <author>Neural Plasticity</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5180524</comments>
            <pubDate>Fri, 02 Sep 2011 04:44:02 +0100</pubDate>
            <guid isPermaLink="false">5180524</guid>        </item>
        <item>
            <title>Genetics and function of neocortical GABAergic interneurons in neurodevelopmental disorders.</title>
            <link>http://www.medworm.com/index.php?rid=5180523&amp;cid=s_36794_25_f&amp;fid=36794&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21876820%26dopt%3DAbstract</link>
            <description>Authors: Rossignol E
    Abstract
    A dysfunction of cortical and limbic GABAergic circuits has been postulated to contribute to multiple neurodevelopmental disorders in humans, including schizophrenia, autism, and epilepsy. In the current paper, I summarize the characteristics that underlie the great diversity of cortical GABAergic interneurons and explore how the multiple roles of these cells in developing and mature circuits might contribute to the aforementioned disorders. Furthermore, I review the tightly controlled genetic cascades that determine the fate of cortical interneurons and summarize how the dysfunction of genes important for the generation, specification, maturation, and function of cortical interneurons might contribute to these disorders.
    PMID: 21876820 [PubMed - i...</description>
            <author>Neural Plasticity</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5180523</comments>
            <pubDate>Fri, 02 Sep 2011 04:44:02 +0100</pubDate>
            <guid isPermaLink="false">5180523</guid>        </item>
        <item>
            <title>Swimming exercise in the acute or late phase after sciatic nerve crush accelerates nerve regeneration.</title>
            <link>http://www.medworm.com/index.php?rid=5180522&amp;cid=s_36794_25_f&amp;fid=36794&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21876821%26dopt%3DAbstract</link>
            <description>Authors: Teodori RM, Betini J, de Oliveira LS, Sobral LL, Takeda SY, Montebelo MI
    Abstract
    There is no consensus about the best time to start exercise after peripheral nerve injury. We evaluated the morphological and functional characteristics of the sciatic nerves of rats that began to swim immediately after crush nerve injury (CS1), those that began to swim 14 days after injury (CS14), injured rats not submitted to swimming (C), and uninjured rats submitted to swimming (S). After 30 days the number of axons in CS1 and CS14 was lower than in C (P &amp;lt; 0.01). The diameter of axons and nerve fibers was larger in CS1 (P &amp;lt; 0.01) and CS14 (P &amp;lt; 0.05) than in C, and myelin sheath thickness was lower in all crushed groups (P &amp;lt; 0.05). There was no functional difference between CS1...</description>
            <author>Neural Plasticity</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5180522</comments>
            <pubDate>Fri, 02 Sep 2011 04:44:02 +0100</pubDate>
            <guid isPermaLink="false">5180522</guid>        </item>
        <item>
            <title>Neurturin Evokes MAPK-Dependent Upregulation of Egr4 and KCC2 in Developing Neurons.</title>
            <link>http://www.medworm.com/index.php?rid=5143719&amp;cid=s_36794_25_f&amp;fid=36794&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21837281%26dopt%3DAbstract</link>
            <description>Authors: Ludwig A, Uvarov P, Pellegrino C, Thomas-Crusells J, Schuchmann S, Saarma M, Airaksinen MS, Rivera C
    Abstract
    The K-Cl cotransporter KCC2 plays a crucial role in the functional development of GABA(A)-mediated responses rendering GABA hyperpolarizing in adult neurons. We have previously shown that BDNF upregulates KCC2 in immature neurons through the transcription factor Egr4. The effect of BDNF on Egr4 and KCC2 was shown to be dependent on the activation of ERK1/2. Here we demonstrate that the trophic factor neurturin can also trigger Egr4 expression and upregulate KCC2 in an ERK1/2-dependent manner. These results show that Egr4 is an important component in the mechanism for trophic factor-mediated upregulation of KCC2 in immature neurons involving the activation of specif...</description>
            <author>Neural Plasticity</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5143719</comments>
            <pubDate>Sat, 20 Aug 2011 14:54:03 +0100</pubDate>
            <guid isPermaLink="false">5143719</guid>        </item>
        <item>
            <title>Correlations between Hippocampal Neurogenesis and Metabolic Indices in Adult Nonhuman Primates.</title>
            <link>http://www.medworm.com/index.php?rid=5143718&amp;cid=s_36794_25_f&amp;fid=36794&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21837282%26dopt%3DAbstract</link>
            <description>This study demonstrates that markers of dentate gyrus neuroplasticity correlate with metabolic parameters in primates.
    PMID: 21837282 [PubMed - in process] (Source: Neural Plasticity)</description>
            <author>Neural Plasticity</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5143718</comments>
            <pubDate>Sat, 20 Aug 2011 14:54:03 +0100</pubDate>
            <guid isPermaLink="false">5143718</guid>        </item>
        <item>
            <title>Evaluating aftereffects of short-duration transcranial random noise stimulation on cortical excitability.</title>
            <link>http://www.medworm.com/index.php?rid=5118232&amp;cid=s_36794_25_f&amp;fid=36794&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21808744%26dopt%3DAbstract</link>
            <description>Authors: Chaieb L, Paulus W, Antal A
    A 10-minute application of highfrequency (100-640 Hz) transcranial random noise stimulation (tRNS) over the primary motor cortex (M1) increases baseline levels of cortical excitability, lasting around 1 hr poststimulation Terney et al. (2008). We have extended previous work demonstrating this effect by decreasing the stimulation duration to 4, 5, and 6 minutes to assess whether a shorter duration of tRNS can also induce a change in cortical excitability. Single-pulse monophasic transcranial magnetic stimulation (TMS) was used to measure baseline levels of cortical excitability before and after tRNS. A 5- and 6-minute tRNS application induced a significant facilitation. 4-minute tRNS produced no significant aftereffects on corticospinal excitabil...</description>
            <author>Neural Plasticity</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5118232</comments>
            <pubDate>Thu, 11 Aug 2011 20:15:02 +0100</pubDate>
            <guid isPermaLink="false">5118232</guid>        </item>
        <item>
            <title>The role of GABAergic inhibition in ocular dominance plasticity.</title>
            <link>http://www.medworm.com/index.php?rid=5118231&amp;cid=s_36794_25_f&amp;fid=36794&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21826276%26dopt%3DAbstract</link>
            <description>Authors: Heimel JA, van Versendaal D, Levelt CN
    During the last decade, we have gained much insight into the mechanisms that open and close a sensitive period of plasticity in the visual cortex. This brings the hope that novel treatments can be developed for brain injuries requiring renewed plasticity potential and neurodevelopmental brain disorders caused by defective synaptic plasticity. One of the central mechanisms responsible for opening the sensitive period is the maturation of inhibitory innervation. Many molecular and cellular events have been identified that drive this developmental process, including signaling through BDNF and IGF-1, transcriptional control by OTX2, maturation of the extracellular matrix, and GABA-regulated inhibitory synapse formation. The mechanisms through...</description>
            <author>Neural Plasticity</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5118231</comments>
            <pubDate>Thu, 11 Aug 2011 20:15:02 +0100</pubDate>
            <guid isPermaLink="false">5118231</guid>        </item>
        <item>
            <title>Altered GABA Signaling in Early Life Epilepsies.</title>
            <link>http://www.medworm.com/index.php?rid=5118230&amp;cid=s_36794_25_f&amp;fid=36794&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21826277%26dopt%3DAbstract</link>
            <description>Authors: Briggs SW, Galanopoulou AS
    The incidence of seizures is particularly high in the early ages of life. The immaturity of inhibitory systems, such as GABA, during normal brain development and its further dysregulation under pathological conditions that predispose to seizures have been speculated to play a major role in facilitating seizures. Seizures can further impair or disrupt GABA(A) signaling by reshuffling the subunit composition of its receptors or causing aberrant reappearance of depolarizing or hyperpolarizing GABA(A) receptor currents. Such effects may not result in epileptogenesis as frequently as they do in adults. Given the central role of GABA(A) signaling in brain function and development, perturbation of its physiological role may interfere with neuronal morpholog...</description>
            <author>Neural Plasticity</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5118230</comments>
            <pubDate>Thu, 11 Aug 2011 20:15:02 +0100</pubDate>
            <guid isPermaLink="false">5118230</guid>        </item>
        <item>
            <title>Diacylglycerol signaling underlies astrocytic ATP release.</title>
            <link>http://www.medworm.com/index.php?rid=5118229&amp;cid=s_36794_25_f&amp;fid=36794&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21826278%26dopt%3DAbstract</link>
            <description>Authors: Mungenast AE
    Astrocytes have the ability to modulate neuronal excitability and synaptic transmission by the release of gliotransmitters. The importance of ATP released downstream of the activation of Gq-coupled receptors has been well established, but the mechanisms by which this release is regulated are unclear. The current work reveals that the elevation of diacylglycerol (DAG) in astrocytes induces vesicular ATP release. Unexpectedly, DAG-induced ATP release was found to be independent of PKC activation, but dependent upon activation of a C1 domain-containing protein. Astrocytes express the C1 domain-containing protein Munc13-1, which has been implicated in neuronal transmitter release, and RNAi-targeted downregulation of Munc13-1 inhibits astrocytic ATP release. These stud...</description>
            <author>Neural Plasticity</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5118229</comments>
            <pubDate>Thu, 11 Aug 2011 20:15:02 +0100</pubDate>
            <guid isPermaLink="false">5118229</guid>        </item>
        <item>
            <title>Molecular mechanisms underlying activity-dependent GABAergic synapse development and plasticity and its implications for neurodevelopmental disorders.</title>
            <link>http://www.medworm.com/index.php?rid=5118228&amp;cid=s_36794_25_f&amp;fid=36794&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21826279%26dopt%3DAbstract</link>
            <description>Authors: Chattopadhyaya B
    GABAergic interneurons are critical for the normal function and development of neural circuits, and their dysfunction is implicated in a large number of neurodevelopmental disorders. Experience and activity-dependent mechanisms play an important role in GABAergic circuit development, also recent studies involve a number of molecular players involved in the process. Emphasizing the molecular mechanisms of GABAergic synapse formation, in particular basket cell perisomatic synapses, this paper draws attention to the links between critical period plasticity, GABAergic synapse maturation, and the consequences of its dysfunction on the development of the nervous system.
    PMID: 21826279 [PubMed - in process] (Source: Neural Plasticity)</description>
            <author>Neural Plasticity</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5118228</comments>
            <pubDate>Thu, 11 Aug 2011 20:15:02 +0100</pubDate>
            <guid isPermaLink="false">5118228</guid>        </item>
        <item>
            <title>Autism: a &quot;critical period&quot; disorder?</title>
            <link>http://www.medworm.com/index.php?rid=5118227&amp;cid=s_36794_25_f&amp;fid=36794&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21826280%26dopt%3DAbstract</link>
            <description>Autism: a &quot;critical period&quot; disorder?
    Neural Plast. 2011;2011:921680
    Authors: Leblanc JJ, Fagiolini M
    Cortical circuits in the brain are refined by experience during critical periods early in postnatal life. Critical periods are regulated by the balance of excitatory and inhibitory (E/I) neurotransmission in the brain during development. There is now increasing evidence of E/I imbalance in autism, a complex genetic neurodevelopmental disorder diagnosed by abnormal socialization, impaired communication, and repetitive behaviors or restricted interests. The underlying cause is still largely unknown and there is no fully effective treatment or cure. We propose that alteration of the expression and/or timing of critical period circuit refinement in primary sensory brain areas may s...</description>
            <author>Neural Plasticity</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5118227</comments>
            <pubDate>Thu, 11 Aug 2011 20:15:02 +0100</pubDate>
            <guid isPermaLink="false">5118227</guid>        </item>
        <item>
            <title>Brain plasticity and disease: a matter of inhibition.</title>
            <link>http://www.medworm.com/index.php?rid=5070611&amp;cid=s_36794_25_f&amp;fid=36794&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21766040%26dopt%3DAbstract</link>
            <description>Authors: Baroncelli L, Braschi C, Spolidoro M, Begenisic T, Maffei L, Sale A
    One major goal in Neuroscience is the development of strategies promoting neural plasticity in the adult central nervous system, when functional recovery from brain disease and injury is limited. New evidence has underscored a pivotal role for cortical inhibitory circuitries in regulating plasticity both during development and in adulthood. This paper summarizes recent findings showing that the inhibition-excitation balance controls adult brain plasticity and is at the core of the pathogenesis of neurodevelopmental disorders like autism, Down syndrome, and Rett syndrome.
    PMID: 21766040 [PubMed - in process] (Source: Neural Plasticity)</description>
            <author>Neural Plasticity</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5070611</comments>
            <pubDate>Thu, 28 Jul 2011 11:45:03 +0100</pubDate>
            <guid isPermaLink="false">5070611</guid>        </item>
        <item>
            <title>Alterations of GABAergic signaling in autism spectrum disorders.</title>
            <link>http://www.medworm.com/index.php?rid=5070610&amp;cid=s_36794_25_f&amp;fid=36794&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21766041%26dopt%3DAbstract</link>
            <description>Authors: Pizzarelli R, Cherubini E
    Autism spectrum disorders (ASDs) comprise a heterogeneous group of pathological conditions, mainly of genetic origin, characterized by stereotyped behavior, marked impairment in verbal and nonverbal communication, social skills, and cognition. Interestingly, in a small number of cases, ASDs are associated with single mutations in genes encoding for neuroligin-neurexin families. These are adhesion molecules which, by regulating transsynaptic signaling, contribute to maintain a proper excitatory/inhibitory (E/I) balance at the network level. Furthermore, GABA, the main inhibitory neurotransmitter in adult life, at late embryonic/early postnatal stages has been shown to depolarize and excite targeted cell through an outwardly directed flux of chloride. T...</description>
            <author>Neural Plasticity</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5070610</comments>
            <pubDate>Thu, 28 Jul 2011 11:45:03 +0100</pubDate>
            <guid isPermaLink="false">5070610</guid>        </item>
        <item>
            <title>GABAergic neuronal precursor grafting: implications in brain regeneration and plasticity.</title>
            <link>http://www.medworm.com/index.php?rid=5070609&amp;cid=s_36794_25_f&amp;fid=36794&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21766042%26dopt%3DAbstract</link>
            <description>Authors: Alvarez Dolado M, Broccoli V
    Numerous neurological disorders are caused by a dysfunction of the GABAergic system that impairs or either stimulates its inhibitory action over its neuronal targets. Pharmacological drugs have generally been proved very effective in restoring its normal function, but their lack of any sort of spatial or cell type specificity has created some limitations in their use. In the last decades, cell-based therapies using GABAergic neuronal grafts have emerged as a promising treatment, since they may restore the lost equilibrium by cellular replacement of the missing/altered inhibitory neurons or modulating the hyperactive excitatory system. In particular, the discovery that embryonic ganglionic eminence-derived GABAergic precursors are able to disperse a...</description>
            <author>Neural Plasticity</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5070609</comments>
            <pubDate>Thu, 28 Jul 2011 11:45:03 +0100</pubDate>
            <guid isPermaLink="false">5070609</guid>        </item>
        <item>
            <title>Functional Consequences of the Disturbances in the GABA-Mediated Inhibition Induced by Injuriesin the Cerebral Cortex.</title>
            <link>http://www.medworm.com/index.php?rid=5070608&amp;cid=s_36794_25_f&amp;fid=36794&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21766043%26dopt%3DAbstract</link>
            <description>Authors: Imbrosci B, Mittmann T
    Cortical injuries are often reported to induce a suppression of the intracortical GABAergic inhibition in the surviving, neighbouring neuronal networks. Since GABAergic transmission provides the main source of inhibition in the mammalian brain, this condition may lead to hyperexcitability and epileptiform activity of cortical networks. However, inhibition plays also a crucial role in limiting the plastic properties of neuronal circuits, and as a consequence, interventions aiming to reestablish a normal level of inhibition might constrain the plastic capacity of the cortical tissue. A promising strategy to minimize the deleterious consequences of a modified inhibitory transmission without preventing the potential beneficial effects on cortical plasticity ...</description>
            <author>Neural Plasticity</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5070608</comments>
            <pubDate>Thu, 28 Jul 2011 11:45:03 +0100</pubDate>
            <guid isPermaLink="false">5070608</guid>        </item>
        <item>
            <title>Spatial and Temporal Dynamics in the Ionic Driving Force for GABA(A) Receptors.</title>
            <link>http://www.medworm.com/index.php?rid=5070607&amp;cid=s_36794_25_f&amp;fid=36794&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21766044%26dopt%3DAbstract</link>
            <description>Authors: Wright R, Raimondo JV, Akerman CJ
    It is becoming increasingly apparent that the strength of GABAergic synaptic transmission is dynamic. One parameter that can establish differences in the actions of GABAergic synapses is the ionic driving force for the chloride-permeable GABA(A) receptor (GABA(A)R). Here we review some of the sophisticated ways in which this ionic driving force can vary within neuronal circuits. This driving force for GABA(A)Rs is subject to tight spatial control, with the distribution of Cl(-) transporter proteins and channels generating regional variation in the strength of GABA(A)R signalling across a single neuron. GABA(A)R dynamics can result from short-term changes in their driving force, which involve the temporary accumulation or depletion of intracell...</description>
            <author>Neural Plasticity</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5070607</comments>
            <pubDate>Thu, 28 Jul 2011 11:45:03 +0100</pubDate>
            <guid isPermaLink="false">5070607</guid>        </item>
        <item>
            <title>Loss of prestin does not alter the development of auditory cortical dendritic spines.</title>
            <link>http://www.medworm.com/index.php?rid=5070606&amp;cid=s_36794_25_f&amp;fid=36794&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21773053%26dopt%3DAbstract</link>
            <description>Authors: Bogart LJ, Levy AD, Gladstone M, Allen PD, Zettel M, Ison JR, Luebke AE, Majewska AK
    Disturbance of sensory input during development can have disastrous effects on the development of sensory cortical areas. To examine how moderate perturbations of hearing can impact the development of primary auditory cortex, we examined markers of excitatory synapses in mice who lacked prestin, a protein responsible for somatic electromotility of cochlear outer hair cells. While auditory brain stem responses of these mice show an approximately 40 dB increase in threshold, we found that loss of prestin produced no changes in spine density or morphological characteristics on apical dendrites of cortical layer 5 pyramidal neurons. PSD-95 immunostaining also showed no changes in overall excitat...</description>
            <author>Neural Plasticity</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5070606</comments>
            <pubDate>Thu, 28 Jul 2011 11:45:03 +0100</pubDate>
            <guid isPermaLink="false">5070606</guid>        </item>
        <item>
            <title>Suspension of mitotic activity in dentate gyrus of the hibernating ground squirrel.</title>
            <link>http://www.medworm.com/index.php?rid=5070605&amp;cid=s_36794_25_f&amp;fid=36794&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21773054%26dopt%3DAbstract</link>
            <description>Authors: Popov VI, Kraev IV, Ignat'ev DA, Stewart MG
    Neurogenesis occurs in the adult mammalian hippocampus, a region of the brain important for learning and memory. Hibernation in Siberian ground squirrels provides a natural model to study mitosis as the rapid fall in body temperature in 24 h (from 35-36°C to +4-6°C) permits accumulation of mitotic cells at different stages of the cell cycle. Histological methods used to study adult neurogenesis are limited largely to fixed tissue, and the mitotic state elucidated depends on the specific phase of mitosis at the time of day. However, using an immunohistochemical study of doublecortin (DCX) and BrdU-labelled neurons, we demonstrate that the dentate gyrus of the ground squirrel hippocampus contains a population of immature cells whic...</description>
            <author>Neural Plasticity</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5070605</comments>
            <pubDate>Thu, 28 Jul 2011 11:45:03 +0100</pubDate>
            <guid isPermaLink="false">5070605</guid>        </item>
        <item>
            <title>Maturation of the GABAergic transmission in normal and pathologic motoneurons.</title>
            <link>http://www.medworm.com/index.php?rid=5070604&amp;cid=s_36794_25_f&amp;fid=36794&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21785735%26dopt%3DAbstract</link>
            <description>Authors: Allain AE, Le Corronc H, Delpy A, Cazenave W, Meyrand P, Legendre P, Branchereau P
    γ-aminobutyric acid (GABA) acting on Cl(-)-permeable ionotropic type A (GABA(A)) receptors (GABA(A)R) is the major inhibitory neurotransmitter in the adult central nervous system of vertebrates. In immature brain structures, GABA exerts depolarizing effects mostly contributing to the expression of spontaneous activities that are instructive for the construction of neural networks but GABA also acts as a potent trophic factor. In the present paper, we concentrate on brainstem and spinal motoneurons that are largely targeted by GABAergic interneurons, and we bring together data on the switch from excitatory to inhibitory effects of GABA, on the maturation of the GABAergic system and GABA(A)R subu...</description>
            <author>Neural Plasticity</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5070604</comments>
            <pubDate>Thu, 28 Jul 2011 11:45:03 +0100</pubDate>
            <guid isPermaLink="false">5070604</guid>        </item>
        <item>
            <title>Assortment of GABAergic plasticity in the cortical interneuron melting pot.</title>
            <link>http://www.medworm.com/index.php?rid=5070603&amp;cid=s_36794_25_f&amp;fid=36794&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21785736%26dopt%3DAbstract</link>
            <description>Authors: Méndez P, Bacci A
    Cortical structures of the adult mammalian brain are characterized by a spectacular diversity of inhibitory interneurons, which use GABA as neurotransmitter. GABAergic neurotransmission is fundamental for integrating and filtering incoming information and dictating postsynaptic neuronal spike timing, therefore providing a tight temporal code used by each neuron, or ensemble of neurons, to perform sophisticated computational operations. However, the heterogeneity of cortical GABAergic cells is associated to equally diverse properties governing intrinsic excitability as well as strength, dynamic range, spatial extent, anatomical localization, and molecular components of inhibitory synaptic connections that they form with pyramidal neurons. Recent studies showe...</description>
            <author>Neural Plasticity</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5070603</comments>
            <pubDate>Thu, 28 Jul 2011 11:45:03 +0100</pubDate>
            <guid isPermaLink="false">5070603</guid>        </item>
        <item>
            <title>The many forms and functions of long term plasticity at GABAergic synapses.</title>
            <link>http://www.medworm.com/index.php?rid=5070602&amp;cid=s_36794_25_f&amp;fid=36794&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21789285%26dopt%3DAbstract</link>
            <description>Authors: Maffei A
    On February 12th 1973, Bliss and Lomo submitted their findings on activity-dependent plasticity of glutamatergic synapses. After this groundbreaking discovery, long-term potentiation (LTP) and depression (LTD) gained center stage in the study of learning, memory, and experience-dependent refinement of neural circuits. While LTP and LTD are extensively studied and their relevance to brain function is widely accepted, new experimental and theoretical work recently demonstrates that brain development and function relies on additional forms of plasticity, some of which occur at nonglutamatergic synapses. The strength of GABAergic synapses is modulated by activity, and new functions for inhibitory synaptic plasticity are emerging. Together with excitatory neurons, inhibito...</description>
            <author>Neural Plasticity</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5070602</comments>
            <pubDate>Thu, 28 Jul 2011 11:45:03 +0100</pubDate>
            <guid isPermaLink="false">5070602</guid>        </item>
        <item>
            <title>The NO-cGMP-PKG Signaling Pathway Coordinately Regulates ERK and ERK-Driven Gene Expression at Pre- and Postsynaptic Sites Following LTP-Inducing Stimulation of Thalamo-Amygdala Synapses</title>
            <link>http://www.medworm.com/index.php?rid=4501414&amp;cid=s_36794_168_f&amp;fid=37050&amp;url=http%3A%2F%2Fwww.hindawi.com%2Fjournals%2Fnp%2F2010%2F540940.html</link>
            <description>Long-term potentiation (LTP) at thalamic input synapses to the lateral nucleus of the amygdala (LA) has been proposed as a cellular mechanism of the formation of auditory fear memories. We have previously shown that signaling via ERK/MAPK in both the LA and the medial division of the medial geniculate nucleus/posterior intralaminar nucleus (MGm/PIN) is critical for LTP at thalamo-LA synapses. Here, we show that LTP-inducing stimulation of thalamo-LA inputs regulates the activation of ERK and the expression of ERK-driven immediate early genes (IEGs) in both the LA and MGm/PIN. Further, we show that pharmacological blockade of NMDAR-driven synaptic plasticity, NOS activation, or PKG signaling in the LA significantly impairs high-frequency stimulation-(HFS-) induced ERK activation and IEG exp...</description>
            <author>Neural Plasticity</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4501414</comments>
            <pubDate>Mon, 21 Feb 2011 18:17:03 +0100</pubDate>
            <guid isPermaLink="false">4501414</guid>        </item>
        <item>
            <title>Systemic Administration of Mesenchymal Stem Cells Increases Neuron Survival after Global Cerebral Ischemia In Vivo (2VO)</title>
            <link>http://www.medworm.com/index.php?rid=4272164&amp;cid=s_36794_168_f&amp;fid=37050&amp;url=http%3A%2F%2Fwww.hindawi.com%2Fjournals%2Fnp%2F2010%2F534925.html</link>
            <description>Although many studies have shown that administration of stem cells after focal cerebral ischemia improves brain damage, very little data are available concerning the damage induced by global cerebral ischemia. The latter causes neuronal death in selectively vulnerable areas, including the hippocampal CA1 region. We tested the hypothesis that intravenous infusion of bone marrowderived stromal cells (mesenchimal stem cells, MSC) reduce brain damage after transient global ischemia. In adult male Sprague-Dawley rats transient global ischemia was induced using bilateral common carotid artery occlusion for 20&amp;#x2009;min in addition to controlled hypotension. Five days after, the animals were anaesthetized with urethane and the brain was fixed, sectioned and stained with hematoxylin-eosin to inve...</description>
            <author>Neural Plasticity</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4272164</comments>
            <pubDate>Mon, 20 Dec 2010 14:44:34 +0100</pubDate>
            <guid isPermaLink="false">4272164</guid>        </item>
        <item>
            <title>Selective Vulnerability of Neurons in Layer II of the Entorhinal Cortex during Aging and Alzheimer&amp;#39;s Disease</title>
            <link>http://www.medworm.com/index.php?rid=4219519&amp;cid=s_36794_168_f&amp;fid=37050&amp;url=http%3A%2F%2Fwww.hindawi.com%2Fjournals%2Fnp%2F2010%2F108190.html</link>
            <description>All neurons are not created equal. Certain cell populations in specific brain regions are more susceptible to age-related changes that initiate regional and system-level dysfunction. In this respect, neurons in layer II of the entorhinal cortex are selectively vulnerable in aging and Alzheimer&amp;#39;s disease (AD). This paper will cover several hypotheses that attempt to account for age-related alterations among this cell population. We consider whether specific developmental, anatomical, or biochemical features of neurons in layer II of the entorhinal cortex contribute to their particular sensitivity to aging and AD. The entorhinal cortex is a functionally heterogeneous environment, and we will also review data suggesting that, within the entorhinal cortex, there is subregional specificity ...</description>
            <author>Neural Plasticity</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4219519</comments>
            <pubDate>Thu, 02 Dec 2010 09:13:15 +0100</pubDate>
            <guid isPermaLink="false">4219519</guid>        </item>
        <item>
            <title>LTP after Stress: Up or Down&amp;#63;</title>
            <link>http://www.medworm.com/index.php?rid=4040359&amp;cid=s_36794_168_f&amp;fid=37050&amp;url=http%3A%2F%2Fwww.hindawi.com%2Fjournals%2Fnp%2F2007%2F093202.abs.html</link>
            <description>When an organism is exposed to a stressful situation, corticosteroid levels in the brain rise. This rise has consequences for behavioral performance, including memory formation. Over the past decades, it has become clear that a rise in corticosteroid level is also accompanied by a reduction in hippocampal long-term potentiation (LTP). Recent studies, however, indicate that stress does not lead to a universal suppression of LTP. Many factors, including the type of stress, the phase of the stress response, the area of investigation, type of LTP, and the life history of the organism determine in which direction LTP will be changed. (Source: Neural Plasticity)</description>
            <author>Neural Plasticity</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4040359</comments>
            <pubDate>Thu, 07 Oct 2010 23:11:11 +0100</pubDate>
            <guid isPermaLink="false">4040359</guid>        </item>
        <item>
            <title>Upregulation of Neurotrophic Factors Selectively in Frontal Cortex in Response to Olfactory Discrimination Learning</title>
            <link>http://www.medworm.com/index.php?rid=4040358&amp;cid=s_36794_168_f&amp;fid=37050&amp;url=http%3A%2F%2Fwww.hindawi.com%2Fjournals%2Fnp%2F2007%2F013427.abs.html</link>
            <description>This study sought to examine whether the previously demonstrated olfactory-learning-task-induced modifications are preceded by suitable changes in the expression of mRNA for neurotrophic factors and in which brain areas this occurs. Rats were trained to discriminate positive cues in pair of odors for a water reward. The relationship between the learning task and local levels of mRNA for brain-derived neurotrophic factor, tyrosine kinase B, nerve growth factor, and neurotrophin-3 in the frontal cortex, hippocampal subregions, and other regions were assessed 24 hours post 
olfactory learning. The olfactory discrimination learning activated production of endogenous neurotrophic factors and induced their signal transduction in the frontal cortex, but not in other brain areas. These findings su...</description>
            <author>Neural Plasticity</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4040358</comments>
            <pubDate>Thu, 07 Oct 2010 23:11:11 +0100</pubDate>
            <guid isPermaLink="false">4040358</guid>        </item>
        <item>
            <title>Morphology of Pyramidal Neurons in the Rat Prefrontal Cortex: Lateralized Dendritic Remodeling by Chronic Stress</title>
            <link>http://www.medworm.com/index.php?rid=4040357&amp;cid=s_36794_168_f&amp;fid=37050&amp;url=http%3A%2F%2Fwww.hindawi.com%2Fjournals%2Fnp%2F2007%2F046276.abs.html</link>
            <description>The prefrontal cortex (PFC) plays an important role in the stress response. We filled pyramidal neurons in PFC layer III with neurobiotin and analyzed dendrites in rats submitted to chronic restraint stress and in controls. 
In the right prelimbic cortex (PL) of controls, apical and distal dendrites were longer than in the left PL. Stress reduced the total length of apical dendrites in right PL and abolished the hemispheric difference. In right infralimbic cortex (IL) of controls, proximal apical dendrites were longer than in left IL, and stress eliminated this hemispheric difference. No hemispheric difference was detected in anterior cingulate cortex (ACx) of controls, but stress reduced apical dendritic length in left ACx. These data demonstrate interhemispheric differences in the morpho...</description>
            <author>Neural Plasticity</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4040357</comments>
            <pubDate>Thu, 07 Oct 2010 23:11:11 +0100</pubDate>
            <guid isPermaLink="false">4040357</guid>        </item>
        <item>
            <title>Stress before Puberty Exerts a Sex- and Age-Related Impact on Auditory and Contextual Fear Conditioning in the Rat</title>
            <link>http://www.medworm.com/index.php?rid=4040356&amp;cid=s_36794_168_f&amp;fid=37050&amp;url=http%3A%2F%2Fwww.hindawi.com%2Fjournals%2Fnp%2F2007%2F071203.abs.html</link>
            <description>In this study, we evaluated the impact of psychogenic stress (exposure to predator odor followed by placement on an elevated platform) experienced before puberty (days 28&amp;#8211;30) on fear memories and hormonal response of male and female rats during adolescence and early adulthood. Stress before puberty impacted in a sex- and age-specific way on the responses to auditory and contextual fear conditioning in adolescence and adulthood: (a) increased conditioned fear to the tone in males during adolescence but not during adulthood; (b) impaired extinction to the tone in adult males; and (c) reduced freezing responses to the context in adolescent females. Stress before puberty did not influence the corticosterone levels 30&amp;#8201;minutes after an additional stressor given in adulthood. These re...</description>
            <author>Neural Plasticity</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4040356</comments>
            <pubDate>Thu, 07 Oct 2010 23:11:11 +0100</pubDate>
            <guid isPermaLink="false">4040356</guid>        </item>
        <item>
            <title>Effects of Methamphetamine on Single Unit Activity in Rat Medial Prefrontal Cortex In Vivo</title>
            <link>http://www.medworm.com/index.php?rid=4040355&amp;cid=s_36794_168_f&amp;fid=37050&amp;url=http%3A%2F%2Fwww.hindawi.com%2Fjournals%2Fnp%2F2007%2F029821.abs.html</link>
            <description>To investigate how neuronal activity in the prefrontal cortex changes in an animal model of schizophrenia, we recorded single unit activity in the medial prefrontal cortex of urethane-anesthetized and awake rats following methamphetamine (MA) administration. Systemic MA injection (4&amp;#x2009;mg/kg, IP) induced inconsistent changes, that is, both enhancement and reduction, in unit discharge rate, with 
a subset of neurons transiently (&amp;#x003C;30&amp;#x2009;min) elevating their activities. The direction of firing rate change was poorly predicted by the mean firing rate or the degree of burst firing during the baseline period. Also, simultaneously recorded units showed opposite directions of firing rate change, indicating that recording location is a poor predictor of the direction of firing rate c...</description>
            <author>Neural Plasticity</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4040355</comments>
            <pubDate>Thu, 07 Oct 2010 23:11:11 +0100</pubDate>
            <guid isPermaLink="false">4040355</guid>        </item>
        <item>
            <title>10th Jubilee Multidisciplinary International Conference of Neuroscience and Biological Psychiatry &amp;#8220;Stress and Behavior&amp;#8221;</title>
            <link>http://www.medworm.com/index.php?rid=4040354&amp;cid=s_36794_168_f&amp;fid=37050&amp;url=http%3A%2F%2Fwww.hindawi.com%2Fjournals%2Fnp%2F2007%2F070929.abs.html</link>
            <description>St. Petersburg (Russia) hosted the 10th Jubilee Multidisciplinary Conference &amp;#x0093;Stress and Behavior&amp;#x0094; during May 16&amp;#x0096;20, 2007. The conference featured many foremost researchers speaking on recent developments on topics such as the role of neural plasticity, memory, learning, genetics, neuromediators, transporters, and steroids in stress research, spanning disciplines from fields ranging from neurogenetics to clinical psychiatry. The conference was attended by 700 delegates from over 40 nations. (Source: Neural Plasticity)</description>
            <author>Neural Plasticity</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4040354</comments>
            <pubDate>Thu, 07 Oct 2010 23:11:11 +0100</pubDate>
            <guid isPermaLink="false">4040354</guid>        </item>
        <item>
            <title>Chronic Fluoxetine Treatment Induces Brain Region-Specific Upregulation of Genes Associated with BDNF-Induced Long-Term Potentiation</title>
            <link>http://www.medworm.com/index.php?rid=4040353&amp;cid=s_36794_168_f&amp;fid=37050&amp;url=http%3A%2F%2Fwww.hindawi.com%2Fjournals%2Fnp%2F2007%2F026496.abs.html</link>
            <description>Several lines of evidence implicate BDNF in the pathogenesis of stress-induced depression and the delayed efficacy of antidepressant drugs. Antidepressant-induced upregulation of BDNF signaling is thought to promote adaptive neuronal plasticity through effects on gene expression, but the effector genes downstream of BDNF has not been identified. Local infusion of BDNF into the dentate gyrus induces a long-term potentiation (BDNF-LTP) of synaptic transmission that requires upregulation of the immediate early gene Arc. Recently, we identified five genes (neuritin, Narp, TIEG1, Carp, and Arl4d) that are coupregulated with Arc during BDNF-LTP. Here, we examined the expression of these genes in the dentate gyrus, hippocampus proper, and prefrontal cortex after antidepressant treatment. We show ...</description>
            <author>Neural Plasticity</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4040353</comments>
            <pubDate>Thu, 07 Oct 2010 23:11:11 +0100</pubDate>
            <guid isPermaLink="false">4040353</guid>        </item>
        <item>
            <title>39th Annual European Brain and Behaviour Society Abstracts</title>
            <link>http://www.medworm.com/index.php?rid=4040352&amp;cid=s_36794_168_f&amp;fid=37050&amp;url=http%3A%2F%2Fwww.hindawi.com%2Fjournals%2Fnp%2F2007%2F023250.abs.html</link>
            <description>The EUROPEAN BRAIN AND BEHAVIOUR SOCIETY has held its 39th Annual
General Meeting in Trieste, in the campus next to the Miramare
castle and its park, co-hosted by SISSA, the International School
for Advanced Studies, and ICTP, the Abdus Salam International
Centre for Theoretical Physics. Alessandro Treves (SISSA) was the
head and inspiration of the Local Organizing committee, supported
by P. Battaglini, L. Chelazzi, M. Diamond and G. Vallortigara. All
approaches relating brain and behaviour were represented at the
meeting, which aimed to further expand the wide spectrum of
previous EBBS AGMs, and to bring together integrative, system,
cognitive, computational neuroscientists. (Source: Neural Plasticity)</description>
            <author>Neural Plasticity</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4040352</comments>
            <pubDate>Thu, 07 Oct 2010 23:11:11 +0100</pubDate>
            <guid isPermaLink="false">4040352</guid>        </item>
        <item>
            <title>The Coexpression of Reelin and Neuronal Nitric Oxide Synthase in a Subpopulation of Dentate Gyrus Neurons Is Downregulated in Heterozygous Reeler Mice</title>
            <link>http://www.medworm.com/index.php?rid=3924585&amp;cid=s_36794_168_f&amp;fid=37050&amp;url=http%3A%2F%2Fwww.hindawi.com%2Fjournals%2Fnp%2F2010%2F130429.html</link>
            <description>Reelin is an extracellular matrix protein expressed in several interneuron subtypes in the hippocampus and dentate gyrus. Neuronal nitric oxide synthase (nNOS) is also expressed by interneurons in these areas. We investigated whether reelin and nNOS are co-localized in the same population of hippocampal interneurons, and whether this colocalization is altered in the heterozygous reeler mouse. We found colocalization of nNOS in reelin-positive cells in the CA1 stratum radiatum and lacunosum moleculare, the CA3 stratum radiatum, and the dentate gyrus subgranular zone, molecular layer, and hilus. In heterozygous reeler mice, the colocalization of nNOS in reelin-positive cells was significantly decreased only in the subgranular zone and molecular layer. The coexpression of reelin and nNOS in s...</description>
            <author>Neural Plasticity</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3924585</comments>
            <pubDate>Thu, 02 Sep 2010 09:44:13 +0100</pubDate>
            <guid isPermaLink="false">3924585</guid>        </item>
        <item>
            <title>Time-dependent expression of arc and zif268 after acquisition of fear conditioning.</title>
            <link>http://www.medworm.com/index.php?rid=3723463&amp;cid=s_36794_25_f&amp;fid=36794&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20592749%26dopt%3DAbstract</link>
            <description>This study explored the temporal expression profiles of these proteins in the rat hippocampus following fear conditioning. We observed a time-dependent increase of Arc protein in the dorsal hippocampus 30-to-90-minute post training, returning to basal levels at 4 h. Zif268 protein levels, however, gradually increased at 30-minute post training before peaking in expression at 60 minute. The timing of hippocampal Arc and zif268 expression coincides with the critical period for protein synthesis-dependent memory consolidation following fear conditioning. However, the expression of Arc protein appears to be driven by context exploration, whereas, zif268 expression may be more specifically related to associative learning. These findings suggest that altered Arc and zif268 expression are related...</description>
            <author>Neural Plasticity</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3723463</comments>
            <pubDate>Sun, 04 Jul 2010 09:06:03 +0100</pubDate>
            <guid isPermaLink="false">3723463</guid>        </item>
        <item>
            <title>Synaptic Remodeling in the Dentate Gyrus, CA3, CA1, Subiculum, and Entorhinal Cortex of Mice: Effects of Deprived Rearing and Voluntary Running.</title>
            <link>http://www.medworm.com/index.php?rid=3612166&amp;cid=s_36794_25_f&amp;fid=36794&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20508828%26dopt%3DAbstract</link>
            <description>We examined if a similar epigenetic effect of rearing environment on adult neuroplastic responses can be found in mice (Mus musculus). We examined synaptic turnover rates in the dentate gyrus, CA3, CA1, subiculum, and entorhinal cortex. No direct effects of deprived rearing on rates of synaptic turnover were found in any of the studied regions. However, adult wheel running had the effect of leveling layer-specific differences in synaptic remodeling in the dentate gyrus, CA3, and CA1, but not in the entorhinal cortex and subiculum of animals of both rearing treatments. Epigenetic effects during juvenile development affected adult neural plasticity in mice, but seemed to be less pronounced than in gerbils.
    PMID: 20508828 [PubMed - in process] (Source: Neural Plasticity)</description>
            <author>Neural Plasticity</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3612166</comments>
            <pubDate>Sun, 30 May 2010 17:57:02 +0100</pubDate>
            <guid isPermaLink="false">3612166</guid>        </item>
        <item>
            <title>Blockade of NR2A-Containing NMDA Receptors Induces Tau Phosphorylation in Rat Hippocampal Slices.</title>
            <link>http://www.medworm.com/index.php?rid=3612165&amp;cid=s_36794_25_f&amp;fid=36794&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20508838%26dopt%3DAbstract</link>
            <description>Authors: Allyson J, Dontigny E, Auberson Y, Cyr M, Massicotte G
    Physiological activation of the N-methyl-D-aspartate (NMDA) subtype of glutamate receptors has been proposed to play a key role in both neuronal cell function and dysfunction. In the present study, we used selective NMDA receptor antagonists to investigate the involvement of NR2A and NR2B subunits in the modulatory effect of basal NMDA receptor activity on the phosphorylation of Tau proteins. We observed, in acute hippocampal slice preparations, that blockade of NR2A-containing NMDA receptors by the NR2A antagonist NVP-AAM077 provoked the hyperphosphorylation of a residue located in the proline-rich domain of Tau (i.e., Ser199). This effect seemed to be Ser199 specific as there was no increase in phosphorylation at Ser262 ...</description>
            <author>Neural Plasticity</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3612165</comments>
            <pubDate>Sun, 30 May 2010 17:57:02 +0100</pubDate>
            <guid isPermaLink="false">3612165</guid>        </item>
        <item>
            <title>Time-Dependent Expression of Arc and Zif268 after Acquisition of Fear Conditioning</title>
            <link>http://www.medworm.com/index.php?rid=3599259&amp;cid=s_36794_168_f&amp;fid=37050&amp;url=http%3A%2F%2Fwww.hindawi.com%2Fjournals%2Fnp%2F2010%2F139891.html</link>
            <description>This study explored the temporal expression profiles of these proteins in the rat hippocampus following fear conditioning. We observed a time-dependent increase of Arc protein in the dorsal hippocampus 30-to-90-minute post training, returning to basal levels at 4 h. Zif268 protein levels, however, gradually increased at 30-minute post training before peaking in expression at 60 minute. The timing of hippocampal Arc and zif268 expression coincides with the critical period for protein synthesis-dependent memory consolidation following fear conditioning. However, the expression of Arc protein appears to be driven by context exploration, whereas, zif268 expression may be more specifically related to associative learning. These findings suggest that altered Arc and zif268 expression are related...</description>
            <author>Neural Plasticity</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3599259</comments>
            <pubDate>Wed, 26 May 2010 15:47:01 +0100</pubDate>
            <guid isPermaLink="false">3599259</guid>        </item>
        <item>
            <title>Synaptic Remodeling in the Dentate Gyrus, CA3, CA1, Subiculum, and Entorhinal Cortex of Mice: Effects of Deprived Rearing and Voluntary Running</title>
            <link>http://www.medworm.com/index.php?rid=3595440&amp;cid=s_36794_168_f&amp;fid=37050&amp;url=http%3A%2F%2Fwww.hindawi.com%2Fjournals%2Fnp%2F2010%2F870573.html</link>
            <description>We examined if a similar epigenetic effect of rearing environment on adult neuroplastic responses can be found in mice (Mus musculus). We examined synaptic turnover rates in the dentate gyrus, CA3, CA1, subiculum, and entorhinal cortex. No direct effects of deprived rearing on rates of synaptic turnover were found in any of the studied regions. However, adult wheel running had the effect of leveling layer-specific differences in synaptic remodeling in the dentate gyrus, CA3, and CA1, but not in the entorhinal cortex and subiculum of animals of both rearing treatments. Epigenetic effects during juvenile development affected adult neural plasticity in mice, but seemed to be less pronounced than in gerbils. (Source: Neural Plasticity)</description>
            <author>Neural Plasticity</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3595440</comments>
            <pubDate>Tue, 25 May 2010 15:42:23 +0100</pubDate>
            <guid isPermaLink="false">3595440</guid>        </item>
        <item>
            <title>Blockade of NR2A-Containing NMDA Receptors Induces Tau Phosphorylation in Rat Hippocampal Slices</title>
            <link>http://www.medworm.com/index.php?rid=3581457&amp;cid=s_36794_168_f&amp;fid=37050&amp;url=http%3A%2F%2Fwww.hindawi.com%2Fjournals%2Fnp%2F2010%2F340168.html</link>
            <description>Physiological activation of the N-methyl-D-aspartate (NMDA) subtype of glutamate receptors has been proposed to play a key role in both neuronal cell function and dysfunction. In the present study, we used selective NMDA receptor antagonists to investigate the involvement of NR2A and NR2B subunits in the modulatory effect of basal NMDA receptor activity on the phosphorylation of Tau proteins. We observed, in acute hippocampal slice preparations, that blockade of NR2A-containing NMDA receptors by the NR2A antagonist NVP-AAM077 provoked the hyperphosphorylation of a residue located in the proline-rich domain of Tau (i.e., Ser199). This effect seemed to be Ser199 specific as there was no increase in phosphorylation at Ser262 and Ser409 residues located in the microtubule-binding and C-termina...</description>
            <author>Neural Plasticity</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3581457</comments>
            <pubDate>Thu, 20 May 2010 15:27:12 +0100</pubDate>
            <guid isPermaLink="false">3581457</guid>        </item>
        <item>
            <title>Repetitive electric stimulation elicits enduring improvement of sensorimotor performance in seniors.</title>
            <link>http://www.medworm.com/index.php?rid=3501795&amp;cid=s_36794_25_f&amp;fid=36794&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20414332%26dopt%3DAbstract</link>
            <description>Authors: Kalisch T, Tegenthoff M, Dinse HR
    Age-related changes occur on all stages of the human somatosensory pathway, thereby deteriorating tactile, haptic, and sensorimotor performance. However, recent studies show that age-related changes are not irreversible but treatable through peripheral stimulation paradigms based on neuroplasticity mechanisms. We here applied repetitive electric stimulation (rES) to the fingers on a bi-weekly basis for 4 weeks to induce enduring amelioration of age-related changes in healthy individuals aged 60-85 years. Tactile, haptic, and motor performance gradually improved over time of intervention. After termination of rES, tactile acuity recovered to baseline within 2 weeks, while the gains in haptic and motor performance were preserved for 2 weeks. Sha...</description>
            <author>Neural Plasticity</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3501795</comments>
            <pubDate>Sat, 24 Apr 2010 20:54:03 +0100</pubDate>
            <guid isPermaLink="false">3501795</guid>        </item>
        <item>
            <title>Repetitive Electric Stimulation Elicits Enduring Improvement of Sensorimotor Performance in Seniors</title>
            <link>http://www.medworm.com/index.php?rid=3467545&amp;cid=s_36794_168_f&amp;fid=37050&amp;url=http%3A%2F%2Fwww.hindawi.com%2Fjournals%2Fnp%2F2010%2F690531.html</link>
            <description>Age-related changes occur on all stages of the human somatosensory pathway, thereby deteriorating tactile, haptic, and sensorimotor performance. However, recent studies show that age-related changes are not irreversible but treatable through peripheral stimulation paradigms based on neuroplasticity mechanisms. We here applied repetitive electric stimulation (rES) to the fingers on a bi-weekly basis for 4 weeks to induce enduring amelioration of age-related changes in healthy individuals aged 60&amp;#x02013;85 years. Tactile, haptic, and motor performance gradually improved over time of intervention. After termination of rES, tactile acuity recovered to baseline within 2 weeks, while the gains in haptic and motor performance were preserved for 2 weeks. Sham stimulation showed no comparable chan...</description>
            <author>Neural Plasticity</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3467545</comments>
            <pubDate>Wed, 14 Apr 2010 16:00:06 +0100</pubDate>
            <guid isPermaLink="false">3467545</guid>        </item>
        <item>
            <title>Plasticity of Horizontal Connections at a Functional Border in Adult Rat Somatosensory Cortex</title>
            <link>http://www.medworm.com/index.php?rid=3326785&amp;cid=s_36794_168_f&amp;fid=37050&amp;url=http%3A%2F%2Fwww.hindawi.com%2Fjournals%2Fnp%2F2009%2F294192.html</link>
            <description>Horizontal connections in superficial cortical layers integrate information across sensory maps by connecting related functional columns. It has been hypothesized that these connections mediate cortical reorganization via synaptic plasticity. However, it is not known if the horizontal connections from discontinuous cortical regions can undergo plasticity in the adult. Here we located the border between two discontinuous cortical representations in vivo and used either pairing or low-frequency stimulation to induce synaptic plasticity in the horizontal connections surrounding this border in vitro. Individual neurons revealed significant and diverse forms of synaptic plasticity for horizontal connections within a continuous representation and discontinuous representations. Interestingly, bot...</description>
            <author>Neural Plasticity</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3326785</comments>
            <pubDate>Wed, 03 Mar 2010 17:01:49 +0100</pubDate>
            <guid isPermaLink="false">3326785</guid>        </item>
        <item>
            <title>High-Dose Glycine Treatment of Refractory Obsessive-Compulsive Disorder and Body Dysmorphic Disorder in a 5-Year Period</title>
            <link>http://www.medworm.com/index.php?rid=3283391&amp;cid=s_36794_168_f&amp;fid=37050&amp;url=http%3A%2F%2Fwww.hindawi.com%2Fjournals%2Fnp%2F2009%2F768398.html</link>
            <description>This paper describes an individual who was diagnosed with obsessive-compulsive disorder (OCD) and body dysmorphic disorder (BDD) at age 17 when education was discontinued. By age 19, he was housebound without social contacts except for parents. Adequate trials of three selective serotonin reuptake inhibitors, two with atypical neuroleptics, were ineffective. Major exacerbations following ear infections involving Group A &amp;#x03B2;-hemolytic streptococcus at ages 19 and 20 led to intravenous immune globulin therapy, which was also ineffective. At age 22, another severe exacerbation followed antibiotic treatment for H. pylori. This led to a hypothesis that postulates deficient signal transduction by the N-methyl-D-aspartate receptor (NMDAR). Treatment with glycine, an NMDAR coagonist, over 5 y...</description>
            <author>Neural Plasticity</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3283391</comments>
            <pubDate>Thu, 18 Feb 2010 16:46:53 +0100</pubDate>
            <guid isPermaLink="false">3283391</guid>        </item>
        <item>
            <title>Directed Fiber Outgrowth from Transplanted Embryonic Cortex-Derived Neurospheres in the Adult Mouse Brain</title>
            <link>http://www.medworm.com/index.php?rid=3270972&amp;cid=s_36794_168_f&amp;fid=37050&amp;url=http%3A%2F%2Fwww.hindawi.com%2Fjournals%2Fnp%2F2009%2F852492.html</link>
            <description>Neural transplantation has emerged as an attractive strategy for the replacement of neurons that have been lost in the central nervous system. Multipotent neural progenitor cells are potentially useful as donor cells to repopulate the degenerated regions. One important aspect of a transplantation strategy is whether transplanted cells are capable of fiber outgrowth with the aim of rebuilding axonal connections within the host brain. To address this issue, we expanded neuronal progenitor from the cortex of embryonic day 15 ubiquitously green fluorescent protein-expressing transgenic mice as neurospheres in vitro and grafted them into the entorhinal cortex of 8-week-old mice immediately after a perforant pathway lesion. After transplantation into a host brain with a lesion of the entorhino-h...</description>
            <author>Neural Plasticity</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3270972</comments>
            <pubDate>Sun, 14 Feb 2010 16:31:30 +0100</pubDate>
            <guid isPermaLink="false">3270972</guid>        </item>
        <item>
            <title>Contributions of Matrix Metalloproteinases to Neural Plasticity, Habituation, Associative Learning and Drug Addiction</title>
            <link>http://www.medworm.com/index.php?rid=3258693&amp;cid=s_36794_168_f&amp;fid=37050&amp;url=http%3A%2F%2Fwww.hindawi.com%2Fjournals%2Fnp%2F2009%2F579382.html</link>
            <description>The premise of this paper is that increased expression of matrix metalloproteinases (MMPs) permits the reconfiguration of synaptic connections (i.e., neural plasticity) by degrading cell adhesion molecules (CAMs) designed to provide stability to those extracellular matrix (ECM) proteins that form scaffolding supporting neurons and glia. It is presumed that while these ECM proteins are weakened, and/or detached, synaptic connections can form resulting in new neural pathways. Tissue inhibitors of metalloproteinases (TIMPs) are designed to deactivate MMPs permitting the reestablishment of CAMs, thus returning the system to a reasonably fixed state. This review considers available findings concerning the roles of MMPs and TIMPs in reorganizing ECM proteins thus facilitating the neural plastici...</description>
            <author>Neural Plasticity</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3258693</comments>
            <pubDate>Wed, 10 Feb 2010 16:58:57 +0100</pubDate>
            <guid isPermaLink="false">3258693</guid>        </item>
        <item>
            <title>5-Lipoxygenase DNA Methylation and mRNA Content in the Brain and Heart of Young and Old Mice</title>
            <link>http://www.medworm.com/index.php?rid=3082994&amp;cid=s_36794_168_f&amp;fid=37050&amp;url=http%3A%2F%2Fwww.hindawi.com%2Fjournals%2Fnp%2F2009%2F209596.html</link>
            <description>The expression of 5-lipoxygenase (5-LOX) is affected by aging and regulated by epigenetic mechanisms including DNA methylation. We used methylation-sensitive restriction endonucleases (AciI, BstUI, HpaII, and HinP1I) to assess 5-LOX DNA methylation in brain and heart tissue samples from young (2 months) and old (22 months) mice. We also measured mRNA content for 5-LOX and the DNA methyltransferases DNMT1 and DNMT3a. In young mice, the 5-LOX mRNA content was significantly greater in the heart compared to the brain; 5-LOX DNA methylation was lower, except in the AciI assay in which it was higher in the heart. Aging decreased 5-LOX mRNA content in the heart and increased it in the brain. Aging also increased 5-LOX DNA methylation and this effect was site- (i.e., enzyme) and tissue-specific. G...</description>
            <author>Neural Plasticity</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3082994</comments>
            <pubDate>Sun, 13 Dec 2009 16:10:21 +0100</pubDate>
            <guid isPermaLink="false">3082994</guid>        </item>
        <item>
            <title>Synapse plasticity in motor, sensory, and limbo-prefrontal cortex areas as measured by degrading axon terminals in an environment model of gerbils (Meriones unguiculatus).</title>
            <link>http://www.medworm.com/index.php?rid=2873983&amp;cid=s_36794_25_f&amp;fid=36794&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19809517%26dopt%3DAbstract</link>
            <description>Authors: Neufeld J, Teuchert-Noodt G, Grafen K, Winter Y, Witte AV
    Still little is known about naturally occurring synaptogenesis in the adult neocortex and related impacts of epigenetic influences. We therefore investigated (pre)synaptic plasticity in various cortices of adult rodents, visualized by secondary lysosome accumulations (LA) in remodeling axon terminals. Twenty-two male gerbils from either enriched (ER) or impoverished rearing (IR) were used for quantification of silver-stained LA. ER-animals showed rather low LA densities in most primary fields, whereas barrel and secondary/associative cortices exhibited higher densities and layer-specific differences. In IR-animals, these differences were evened out or even inverted. Basic plastic capacities might be linked with remodeli...</description>
            <author>Neural Plasticity</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2873983</comments>
            <pubDate>Fri, 09 Oct 2009 09:54:02 +0100</pubDate>
            <guid isPermaLink="false">2873983</guid>        </item>
        <item>
            <title>Synapse Plasticity in Motor, Sensory, and Limbo-Prefrontal Cortex Areas as Measured by Degrading Axon Terminals in an Environment Model of Gerbils (Meriones unguiculatus)</title>
            <link>http://www.medworm.com/index.php?rid=2838767&amp;cid=s_36794_168_f&amp;fid=37050&amp;url=http%3A%2F%2Fwww.hindawi.com%2Fjournals%2Fnp%2F2009%2F281561.html</link>
            <description>Still little is known about naturally occurring synaptogenesis in the adult neocortex and related impacts of epigenetic influences. We therefore investigated (pre)synaptic plasticity in various cortices of adult rodents, visualized by secondary lysosome accumulations (LA) in remodeling axon terminals. Twenty-two male gerbils from either enriched (ER) or impoverished rearing (IR) were used for quantification of silver-stained LA. ER-animals showed rather low LA densities in most primary fields, whereas barrel and secondary/associative cortices exhibited higher densities and layer-specific differences. In IR-animals, these differences were evened out or even inverted. Basic plastic capacities might be linked with remodeling of local intrinsic circuits in the context of cortical map adaptatio...</description>
            <author>Neural Plasticity</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2838767</comments>
            <pubDate>Mon, 28 Sep 2009 18:43:06 +0100</pubDate>
            <guid isPermaLink="false">2838767</guid>        </item>
        <item>
            <title>A plastic temporal brain code for conscious state generation.</title>
            <link>http://www.medworm.com/index.php?rid=2661340&amp;cid=s_36794_25_f&amp;fid=36794&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19644552%26dopt%3DAbstract</link>
            <description>Authors: Dresp-Langley B, Durup J
    Consciousness is known to be limited in processing capacity and often described in terms of a unique processing stream across a single dimension: time. In this paper, we discuss a purely temporal pattern code, functionally decoupled from spatial signals, for conscious state generation in the brain. Arguments in favour of such a code include Dehaene et al.'s long-distance reverberation postulate, Ramachandran's remapping hypothesis, evidence for a temporal coherence index and coincidence detectors, and Grossberg's Adaptive Resonance Theory. A time-bin resonance model is developed, where temporal signatures of conscious states are generated on the basis of signal reverberation across large distances in highly plastic neural circuits. The temporal signatu...</description>
            <author>Neural Plasticity</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2661340</comments>
            <pubDate>Sun, 02 Aug 2009 07:58:02 +0100</pubDate>
            <guid isPermaLink="false">2661340</guid>        </item>
        <item>
            <title>Comparison and Regulation of Neuronal Synchronization for Various STDP Rules.</title>
            <link>http://www.medworm.com/index.php?rid=2649549&amp;cid=s_36794_25_f&amp;fid=36794&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19636433%26dopt%3DAbstract</link>
            <description>Authors: Ruan Y, Zhao G
    We discuss effects of various experimentally supported STDP learning rules on frequency synchronization of two unidirectional coupled neurons systematically. First, we show that synchronization windows for all STDP rules cannot be enhanced compared to constant connection under the same model. Then, we explore the influence of learning parameters on synchronization window and find optimal parameters that lead to the widest window. Our findings indicate that synchronization strongly depends on the specific shape and the parameters of the STDP update rules. Thus, we give some explanations by analyzing the synchronization mechanisms for various STDP rules finally.
    PMID: 19636433 [PubMed - in process] (Source: Neural Plasticity)</description>
            <author>Neural Plasticity</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2649549</comments>
            <pubDate>Wed, 29 Jul 2009 15:26:03 +0100</pubDate>
            <guid isPermaLink="false">2649549</guid>        </item>
        <item>
            <title>A Plastic Temporal Brain Code for Conscious State Generation</title>
            <link>http://www.medworm.com/index.php?rid=2625810&amp;cid=s_36794_168_f&amp;fid=37050&amp;url=http%3A%2F%2Fwww.hindawi.com%2Fjournals%2Fnp%2F2009%2F482696.html</link>
            <description>Consciousness is known to be limited in processing capacity and often described in terms of a unique processing stream across a single dimension: time. In this paper, we discuss a purely temporal pattern code, functionally decoupled from spatial signals, for conscious state generation in the brain. Arguments in favour of such a code include Dehaene et al.&amp;#39;s long-distance reverberation postulate, Ramachandran&amp;#39;s remapping hypothesis, evidence for a temporal coherence index and coincidence detectors, and Grossberg&amp;#39;s Adaptive Resonance Theory. A time-bin resonance model is developed, where temporal signatures of conscious states are generated on the basis of signal reverberation across large distances in highly plastic neural circuits. The temporal signatures are delivered by neura...</description>
            <author>Neural Plasticity</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2625810</comments>
            <pubDate>Wed, 22 Jul 2009 12:29:10 +0100</pubDate>
            <guid isPermaLink="false">2625810</guid>        </item>
        <item>
            <title>Comparison and Regulation of Neuronal Synchronization for Various STDP Rules</title>
            <link>http://www.medworm.com/index.php?rid=2605812&amp;cid=s_36794_168_f&amp;fid=37050&amp;url=http%3A%2F%2Fwww.hindawi.com%2Fjournals%2Fnp%2F2009%2F704075.html</link>
            <description>We discuss effects of various experimentally supported STDP learning rules on frequency synchronization of two unidirectional coupled neurons systematically. First, we show that synchronization windows for all STDP rules cannot be enhanced compared to constant connection under the same model. Then, we explore the influence of learning parameters on synchronization window and find optimal parameters that lead to the widest window. Our findings indicate that synchronization strongly depends on the specific shape and the parameters of the STDP update rules. Thus, we give some explanations by analyzing the synchronization mechanisms for various STDP rules finally. (Source: Neural Plasticity)</description>
            <author>Neural Plasticity</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2605812</comments>
            <pubDate>Thu, 16 Jul 2009 12:22:42 +0100</pubDate>
            <guid isPermaLink="false">2605812</guid>        </item>
        <item>
            <title>Viral vector induction of CREB expression in the periaqueductal gray induces a predator stress-like pattern of changes in pCREB expression, neuroplasticity, and anxiety in rodents.</title>
            <link>http://www.medworm.com/index.php?rid=2534895&amp;cid=s_36794_25_f&amp;fid=36794&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19360104%26dopt%3DAbstract</link>
            <description>Authors: Adamec R, Berton O, Abdul Razek W
    Predator stress is lastingly anxiogenic. Phosphorylation of CREB to pCREB (phosphorylated cyclic AMP response element binding protein) is increased after predator stress in fear circuitry, including in the right lateral column of the PAG (periaqueductal gray). Predator stress also potentiates right but not left CeA-PAG (central amygdala-PAG) transmission up to 12 days after stress. The present study explored the functional significance of pCREB changes by increasing CREB expression in non-predator stressed rats through viral vectoring, and assessing the behavioral, electrophysiological and pCREB expression changes in comparison with handled and predator stressed controls. Increasing CREB expression in right PAG was anxiogenic in the elevated p...</description>
            <author>Neural Plasticity</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2534895</comments>
            <pubDate>Sat, 27 Jun 2009 18:13:02 +0100</pubDate>
            <guid isPermaLink="false">2534895</guid>        </item>
        <item>
            <title>Visual deprivation decreases somatic GAD65 puncta number on layer 2/3 pyramidal neurons in mouse visual cortex.</title>
            <link>http://www.medworm.com/index.php?rid=2534893&amp;cid=s_36794_25_f&amp;fid=36794&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19503840%26dopt%3DAbstract</link>
            <description>Authors: Kreczko A, Goel A, Song L, Lee HK
    Proper functioning of the visual system depends on maturation of both excitatory and inhibitory synapses within the visual cortex. Considering that perisomatic inhibition is one of the key factors that control the critical period in visual cortex, it is pertinent to understand its regulation by visual experience. To do this, we developed an immunohistochemical method that allows three-dimensional (3D) analysis of the glutamic acid decarboxylase (GAD) 65-positive inhibitory terminals in the visual cortex. Using this method on transgenic mice expressing yellow fluorescence protein (YFP) in a subset of neurons, we found that the number of somatic GAD65-puncta on individual layer 2/3 pyramidal neurons is reduced when mice are dark-reared from birt...</description>
            <author>Neural Plasticity</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2534893</comments>
            <pubDate>Sat, 27 Jun 2009 18:13:02 +0100</pubDate>
            <guid isPermaLink="false">2534893</guid>        </item>
        <item>
            <title>Autobiographical Memory Retrieval and Hippocampal Activation as a Function of Repetition and the Passage of Time</title>
            <link>http://www.medworm.com/index.php?rid=2468861&amp;cid=s_36794_168_f&amp;fid=37050&amp;url=http%3A%2F%2Fwww.hindawi.com%2Fjournals%2Fnp%2F2007%2F090472.abs.html</link>
            <description>Multiple trace theory (MTT) predicts that hippocampal memory traces expand and strengthen as a function of repeated memory retrievals. We tested this hypothesis utilizing fMRI, comparing the effect of memory retrieval versus the mere passage of time on hippocampal activation. While undergoing fMRI scanning, participants retrieved remote autobiographical memories that had been previously retrieved either one month earlier, two days earlier, or multiple times during the preceding month. Behavioral analyses revealed that the number and consistency of memory details retrieved increased with multiple retrievals but not with the passage of time. While all three retrieval conditions activated a similar set of brain regions normally associated with autobiographical memory retrieval including media...</description>
            <author>Neural Plasticity</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2468861</comments>
            <pubDate>Wed, 10 Jun 2009 07:02:40 +0100</pubDate>
            <guid isPermaLink="false">2468861</guid>        </item>
        <item>
            <title>Abstracts of the 16th Annual Meeting of The Israel Society for Neuroscience: Eilat, Israel, November 25&amp;#8211;27, 2007</title>
            <link>http://www.medworm.com/index.php?rid=2468860&amp;cid=s_36794_168_f&amp;fid=37050&amp;url=http%3A%2F%2Fwww.hindawi.com%2Fjournals%2Fnp%2F2007%2F030585.abs.html</link>
            <description>The Israel Society for Neuroscience&amp;#8212;ISFN&amp;#8212;was founded in 1993 by a
group of Israeli leading scientists conducting research in the
area of neurobiology. The primary goal of the society was to
promote and disseminate the knowledge and understanding acquired
by its members, and to strengthen interactions between them. Since
then, the society holds its annual meeting every year in Eilat
usually during December. At this annual meetings, the
senior Israeli neurobiologists, their teams, and their graduate
students, as well as foreign scientists and students, present
their recent research findings in platform and poster
presentations, and the program of the meeting is mainly based on
the 338 received abstracts which are published in this volume. The
meeting also offers the opportunity f...</description>
            <author>Neural Plasticity</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2468860</comments>
            <pubDate>Wed, 10 Jun 2009 07:02:40 +0100</pubDate>
            <guid isPermaLink="false">2468860</guid>        </item>
        <item>
            <title>Blockade of Cochlear NMDA Receptors Prevents Long-Term Tinnitus during a Brief Consolidation Window after Acoustic Trauma</title>
            <link>http://www.medworm.com/index.php?rid=2468859&amp;cid=s_36794_168_f&amp;fid=37050&amp;url=http%3A%2F%2Fwww.hindawi.com%2Fjournals%2Fnp%2F2007%2F080904.abs.html</link>
            <description>Tinnitus, the perception of sound in the absence of external acoustic stimulation, is a common and devastating pathology. It is often a consequence of acoustic trauma or drug toxicity. The neuronal mechanisms of tinnitus are neither yet fully understood nor are effective treatments available. Using a novel behavioral paradigm for measuring tinnitus in the rat based on tone-guided navigation, we show here that the development of long-term noise-induced tinnitus, the most prevalent and clinically important form of human tinnitus, can be abated by local administration of the NMDA antagonist &amp;#8220;ifenprodil&amp;#8221; into the cochlea in the first 4 days following the noise insult but not afterwards. This suggests that long-term tinnitus undergoes a consolidation-like process, resembling the ont...</description>
            <author>Neural Plasticity</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2468859</comments>
            <pubDate>Wed, 10 Jun 2009 07:02:40 +0100</pubDate>
            <guid isPermaLink="false">2468859</guid>        </item>
        <item>
            <title>Exposure to Forced Swim Stress Alters Local Circuit Activity and Plasticity in the Dentate Gyrus of the Hippocampus</title>
            <link>http://www.medworm.com/index.php?rid=2468858&amp;cid=s_36794_168_f&amp;fid=37050&amp;url=http%3A%2F%2Fwww.hindawi.com%2Fjournals%2Fnp%2F2008%2F194097.html</link>
            <description>Studies have shown that, depending on its severity and context, stress can affect neural plasticity. Most related studies focused on synaptic plasticity and long-term potentiation (LTP) of principle cells. However, evidence suggests that following high-frequency stimulation, which induces LTP in principal cells, modifications also take place at the level of complex interactions with interneurons within the dentate gyrus, that is, at the local circuit level. So far, the possible effects of stress on local circuit activity and plasticity were not studied. Therefore, we set out to examine the possible alterations in local circuit activity and plasticity following exposure to stress. Local circuit activity and plasticity were measured by using frequency dependant inhibition (FDI) and commissur...</description>
            <author>Neural Plasticity</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2468858</comments>
            <pubDate>Wed, 10 Jun 2009 07:02:40 +0100</pubDate>
            <guid isPermaLink="false">2468858</guid>        </item>
        <item>
            <title>Enhancement of Neocortical-Medial Temporal EEG Correlations during Non-REM Sleep</title>
            <link>http://www.medworm.com/index.php?rid=2468857&amp;cid=s_36794_168_f&amp;fid=37050&amp;url=http%3A%2F%2Fwww.hindawi.com%2Fjournals%2Fnp%2F2008%2F563028.html</link>
            <description>Interregional interactions of oscillatory activity are crucial for the integrated processing of multiple brain regions. However, while the EEG in virtually all brain structures passes through substantial modifications during sleep, it is still an open question whether interactions between neocortical and medial temporal EEG oscillations also depend on the state of alertness. Several previous studies in animals and humans suggest that hippocampal-neocortical interactions crucially depend on the state of alertness (i.e., waking state or sleep). Here, we analyzed scalp and intracranial EEG recordings during sleep and waking state in epilepsy patients undergoing presurgical evaluation. We found that the amplitudes of oscillations within the medial temporal lobe and the neocortex were more clos...</description>
            <author>Neural Plasticity</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2468857</comments>
            <pubDate>Wed, 10 Jun 2009 07:02:40 +0100</pubDate>
            <guid isPermaLink="false">2468857</guid>        </item>
        <item>
            <title>The Role of the Entorhinal Cortex in Extinction: Influences of Aging</title>
            <link>http://www.medworm.com/index.php?rid=2468856&amp;cid=s_36794_168_f&amp;fid=37050&amp;url=http%3A%2F%2Fwww.hindawi.com%2Fjournals%2Fnp%2F2008%2F595282.html</link>
            <description>The entorhinal cortex is perhaps the area of the brain in which neurofibrillary tangles and amyloid plaques are first detectable in old age with or without mild cognitive impairment, and very particularly in Alzheimer&amp;#39;s disease. It plays a key role in memory formation, retrieval, and extinction, as part of circuits that include the hippocampus, the amygdaloid nucleus, and several regions of the neocortex, in particular of the prefrontal cortex. Lesions or biochemical impairments of the entorhinal cortex hinder extinction. Microinfusion experiments have shown that glutamate NMDA receptors, calcium and calmodulin-dependent protein kinase II, and protein synthesis in the entorhinal cortex are involved in and required for extinction. Aging also hinders extinction; it is possible that its e...</description>
            <author>Neural Plasticity</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2468856</comments>
            <pubDate>Wed, 10 Jun 2009 07:02:40 +0100</pubDate>
            <guid isPermaLink="false">2468856</guid>        </item>
        <item>
            <title>Differential Induction of Long-Term Potentiation in the Horizontal versus Columnar Superficial Connections to Layer II Cells of the Entorhinal Cortex</title>
            <link>http://www.medworm.com/index.php?rid=2468855&amp;cid=s_36794_168_f&amp;fid=37050&amp;url=http%3A%2F%2Fwww.hindawi.com%2Fjournals%2Fnp%2F2008%2F814815.html</link>
            <description>The entorhinal cortex (EC) is a nodal and independent mnemonic element of the medial temporal lobe memory circuit as it forms a bidirectional interface between the neocortex and hippocampus. Within the EC, intra- and inter-lamellar associational connections occur via horizontal and columnar projections, respectively. We undertook a comparative study of these two inputs as they converge upon EC layer II cells using whole-cell patch techniques in an adult rat EC horizontal slice preparation in which the deepest layers (V-VI) had been dissected out. Electrical stimulation of layers I and III during GABA blockade allowed us to study excitatory synaptic properties and plasticity in the horizontal and columnar fibre systems, respectively. Both pathways exhibited AMPA- and NMDA-receptor mediated ...</description>
            <author>Neural Plasticity</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2468855</comments>
            <pubDate>Wed, 10 Jun 2009 07:02:40 +0100</pubDate>
            <guid isPermaLink="false">2468855</guid>        </item>
        <item>
            <title>Effect of Prenatal Protein Malnutrition on Long-Term Potentiation and BDNF Protein Expression in the Rat Entorhinal Cortex after Neocortical and Hippocampal Tetanization</title>
            <link>http://www.medworm.com/index.php?rid=2468854&amp;cid=s_36794_168_f&amp;fid=37050&amp;url=http%3A%2F%2Fwww.hindawi.com%2Fjournals%2Fnp%2F2008%2F646919.html</link>
            <description>Reduction of the protein content from 25 to 8&amp;#37; casein in the diet of pregnant rats results in impaired neocortical long-term potentiation (LTP) of the offspring together with lower visuospatial memory performance. The present study was aimed to investigate whether this type of maternal malnutrition could result in modification of plastic capabilities of the entorhinal cortex (EC) in the adult progeny. Unlike normal eutrophic controls, 55&amp;#8211;60-day-old prenatally malnourished rats were unable to develop LTP in the medial EC to tetanizing stimulation delivered to either the ipsilateral occipital cortex or the CA1 hippocampal region. Tetanizing stimulation of CA1 also failed to increase the concentration of brain-derived neurotrophic factor (BDNF) in the EC of 
malnourished rats. Impai...</description>
            <author>Neural Plasticity</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2468854</comments>
            <pubDate>Wed, 10 Jun 2009 07:02:40 +0100</pubDate>
            <guid isPermaLink="false">2468854</guid>        </item>
        <item>
            <title>Complementary Roles of Hippocampus and Medial Entorhinal Cortex in Episodic Memory</title>
            <link>http://www.medworm.com/index.php?rid=2468853&amp;cid=s_36794_168_f&amp;fid=37050&amp;url=http%3A%2F%2Fwww.hindawi.com%2Fjournals%2Fnp%2F2008%2F258467.html</link>
            <description>Spatial mapping and navigation are figured prominently in the extant literature that describes hippocampal function. The medial entorhinal cortex is likewise attracting increasing interest, insofar as evidence accumulates that this area also contributes to spatial information processing. Here, we discuss recent electrophysiological findings that offer an alternate view of hippocampal and medial entorhinal function. These findings suggest complementary contributions of the hippocampus and medial entorhinal cortex in support of episodic memory, wherein hippocampal networks encode sequences of events that compose temporally and spatially extended episodes, whereas medial entorhinal networks disambiguate overlapping episodes by binding sequential events into distinct memories. (Source: Neural ...</description>
            <author>Neural Plasticity</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2468853</comments>
            <pubDate>Wed, 10 Jun 2009 07:02:40 +0100</pubDate>
            <guid isPermaLink="false">2468853</guid>        </item>
        <item>
            <title>Spontaneous Plasticity of Multineuronal Activity Patterns in Activated Hippocampal Networks</title>
            <link>http://www.medworm.com/index.php?rid=2468852&amp;cid=s_36794_168_f&amp;fid=37050&amp;url=http%3A%2F%2Fwww.hindawi.com%2Fjournals%2Fnp%2F2008%2F108969.html</link>
            <description>Using functional multineuron imaging with single-cell resolution, we examined how hippocampal networks by themselves change the spatiotemporal patterns of spontaneous activity during the course of emitting spontaneous activity. When extracellular ionic concentrations were changed to those that mimicked in vivo conditions, spontaneous activity was increased in active cell number and activity frequency. When ionic compositions were restored to the control conditions, the activity level returned to baseline, but the weighted spatial dispersion of active cells, as assessed by entropy-based metrics, did not. Thus, the networks can modify themselves by altering the internal structure of their correlated activity, even though they as a whole maintained the same level of activity in space and time...</description>
            <author>Neural Plasticity</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2468852</comments>
            <pubDate>Wed, 10 Jun 2009 07:02:40 +0100</pubDate>
            <guid isPermaLink="false">2468852</guid>        </item>
        <item>
            <title>Linking Cellular Mechanisms to Behavior: Entorhinal Persistent Spiking and Membrane Potential Oscillations May Underlie Path Integration, Grid Cell Firing, and Episodic Memory</title>
            <link>http://www.medworm.com/index.php?rid=2468851&amp;cid=s_36794_168_f&amp;fid=37050&amp;url=http%3A%2F%2Fwww.hindawi.com%2Fjournals%2Fnp%2F2008%2F658323.html</link>
            <description>This article reviews physiological data on persistent spiking and membrane potential oscillations in entorhinal cortex then presents models showing how both these cellular mechanisms could contribute to properties observed during unit recording, including grid cell firing, and how they could underlie behavioural functions including path integration. The interaction of oscillations and persistent firing could contribute to encoding and retrieval of trajectories through space and time as a mechanism relevant to episodic memory. (Source: Neural Plasticity)</description>
            <author>Neural Plasticity</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2468851</comments>
            <pubDate>Wed, 10 Jun 2009 07:02:40 +0100</pubDate>
            <guid isPermaLink="false">2468851</guid>        </item>
        <item>
            <title>Postsynaptic Signals Mediating Induction of Long-Term Synaptic Depression in the Entorhinal Cortex</title>
            <link>http://www.medworm.com/index.php?rid=2468850&amp;cid=s_36794_168_f&amp;fid=37050&amp;url=http%3A%2F%2Fwww.hindawi.com%2Fjournals%2Fnp%2F2008%2F840374.html</link>
            <description>The entorhinal cortex receives a large projection from the piriform cortex, and synaptic plasticity in this pathway may affect olfactory processing. In vitro whole cell recordings have been used here to investigate postsynaptic signalling mechanisms that mediate the induction of long-term synaptic depression (LTD) in layer II entorhinal cortex cells. To induce LTD, pairs of pulses, using a 30-millisecond interval, were delivered at 1&amp;#x2009;Hz for 15&amp;#x2009;minutes. Induction of LTD was blocked by the NMDA receptor antagonist APV and by the calcium chelator BAPTA, consistent with a requirement for calcium influx via NMDA receptors. Induction of LTD was blocked when the FK506 was included in the intracellular solution to block the phosphatase calcineurin. Okadaic acid, which blocks activati...</description>
            <author>Neural Plasticity</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2468850</comments>
            <pubDate>Wed, 10 Jun 2009 07:02:40 +0100</pubDate>
            <guid isPermaLink="false">2468850</guid>        </item>
        <item>
            <title>Dopaminergic Suppression of Synaptic Transmission in the Lateral Entorhinal Cortex</title>
            <link>http://www.medworm.com/index.php?rid=2468849&amp;cid=s_36794_168_f&amp;fid=37050&amp;url=http%3A%2F%2Fwww.hindawi.com%2Fjournals%2Fnp%2F2008%2F203514.html</link>
            <description>Dopaminergic projections to the superficial layers of the lateral entorhinal cortex can modulate the strength of olfactory inputs to the region. We have found that low concentrations of dopamine facilitate field EPSPs in the entorhinal cortex, and that higher concentrations of dopamine suppress synaptic responses. Here, we have used whole-cell current clamp recordings from layer II neurons to determine the mechanisms of the suppression. Dopamine (10 to 50&amp;#x2009;&amp;#x03BC;M)
hyperpolarized membrane potential and reversibly suppressed the amplitude of EPSPs evoked by layer I stimulation. Both AMPA- and NMDA-mediated components were suppressed, and paired-pulse facilitation was also enhanced indicating that the suppression is mediated largely by reduced glutamate release. Blockade of D2-like r...</description>
            <author>Neural Plasticity</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2468849</comments>
            <pubDate>Wed, 10 Jun 2009 07:02:40 +0100</pubDate>
            <guid isPermaLink="false">2468849</guid>        </item>
        <item>
            <title>What Does the Anatomical Organization of the Entorhinal Cortex Tell Us?</title>
            <link>http://www.medworm.com/index.php?rid=2468848&amp;cid=s_36794_168_f&amp;fid=37050&amp;url=http%3A%2F%2Fwww.hindawi.com%2Fjournals%2Fnp%2F2008%2F381243.html</link>
            <description>The entorhinal cortex is commonly perceived as a major input and output structure of the hippocampal formation, entertaining the role of the nodal point of cortico-hippocampal circuits. Superficial layers receive convergent cortical information, which is relayed to structures in the hippocampus, and hippocampal output reaches deep layers of entorhinal cortex, that project back to the cortex. The finding of the grid cells in all layers and reports on interactions between deep and superficial layers  indicate that this rather simplistic perception may be at fault. Therefore, an integrative approach on the entorhinal cortex, that takes into account recent additions to our knowledge database on entorhinal connectivity, is timely. We argue that layers in entorhinal cortex show different functio...</description>
            <author>Neural Plasticity</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2468848</comments>
            <pubDate>Wed, 10 Jun 2009 07:02:40 +0100</pubDate>
            <guid isPermaLink="false">2468848</guid>        </item>
        <item>
            <title>The Role of NMDA Receptor Subtypes in Short-Term Plasticity in the Rat Entorhinal Cortex</title>
            <link>http://www.medworm.com/index.php?rid=2468847&amp;cid=s_36794_168_f&amp;fid=37050&amp;url=http%3A%2F%2Fwww.hindawi.com%2Fjournals%2Fnp%2F2008%2F872456.html</link>
            <description>We have previously shown that spontaneous release of glutamate in the entorhinal cortex (EC) is tonically facilitated via activation of presynaptic NMDA receptors 
 (NMDAr) containing the NR2B subunit. Here we show that the same receptors mediate short-term plasticity manifested by frequency-dependent facilitation of evoked glutamate release at these synapses. Whole-cell patch-clamp recordings were made from layer V pyramidal neurones in rat EC slices. Evoked excitatory postsynaptic currents showed strong facilitation at relatively low frequencies (3&amp;#x2009;Hz) of activation. Facilitation was abolished by an NR2B-selective blocker (Ro 25-6981), but unaffected by NR2A-selective antagonists (Zn2+, NVP-AAM077). In contrast, postsynaptic NMDAr-mediated responses could be reduced by subunit-sel...</description>
            <author>Neural Plasticity</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2468847</comments>
            <pubDate>Wed, 10 Jun 2009 07:02:40 +0100</pubDate>
            <guid isPermaLink="false">2468847</guid>        </item>
        <item>
            <title>The Role of GLUK5-Containing Kainate Receptors in Entorhinal Cortex Gamma Frequency Oscillations</title>
            <link>http://www.medworm.com/index.php?rid=2468846&amp;cid=s_36794_168_f&amp;fid=37050&amp;url=http%3A%2F%2Fwww.hindawi.com%2Fjournals%2Fnp%2F2008%2F401645.html</link>
            <description>Using in vitro brain slices of hippocampus and cortex, neuronal oscillations in the frequency range of 30&amp;#8211;80&amp;#x2009;Hz (gamma frequency oscillations) can be induced by a number of pharmacological manipulations. The most routinely used is the bath application of the broad-spectrum glutamate receptor agonist, kainic acid. In the hippocampus, work using transgenic kainate receptor knockout mice have revealed information about the specific subunit composition of the kainate receptor implicated in the generation and maintenance of the gamma frequency oscillation. However, there is a paucity of such detail regarding gamma frequency oscillation in the cortex. Using specific pharmacological agonists and antagonists for the kainate receptor, we have set out to examine the contribution of kain...</description>
            <author>Neural Plasticity</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2468846</comments>
            <pubDate>Wed, 10 Jun 2009 07:02:40 +0100</pubDate>
            <guid isPermaLink="false">2468846</guid>        </item>
        <item>
            <title>Understanding Stress-Related Behavioral Phenotypes: Report from the 1st International Neuroscience Summer School and the 11th International &amp;#8220;Stress and Behavior&amp;#8221; Conference</title>
            <link>http://www.medworm.com/index.php?rid=2468845&amp;cid=s_36794_168_f&amp;fid=37050&amp;url=http%3A%2F%2Fwww.hindawi.com%2Fjournals%2Fnp%2F2008%2F543075.html</link>
            <description>The 1st International Neuroscience Summer School and the 11th International Multidisciplinary Neuroscience and Biopsychiatry Conference on Stress and Behavior were held in St. Petersburg, Russia, during May 9&amp;#8211;20, 2008. The summer school gathered 30 talented young scientists from 15 countries worldwide, and was dedicated to different topics of behavioral neuroscience. Many interactive courses were provided on neuropharmacology, animal phenotyping, and biopsychology. The conference&amp;#39;s excellent scientific and social program attracted almost 500 delegates from 40 countries from many areas of stress research. The eclectic interaction between medical doctors, basic scientists, psychologists, and students made for a productive and collaborative environment, which contributed greatly to ...</description>
            <author>Neural Plasticity</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2468845</comments>
            <pubDate>Wed, 10 Jun 2009 07:02:40 +0100</pubDate>
            <guid isPermaLink="false">2468845</guid>        </item>
        <item>
            <title>Modulation of Network Oscillatory Activity and GABAergic Synaptic Transmission by CB1 Cannabinoid Receptors in the Rat Medial Entorhinal Cortex</title>
            <link>http://www.medworm.com/index.php?rid=2468844&amp;cid=s_36794_168_f&amp;fid=37050&amp;url=http%3A%2F%2Fwww.hindawi.com%2Fjournals%2Fnp%2F2008%2F808564.html</link>
            <description>We report that arachidonylcyclopropylamide (ACPA; 10&amp;#x2009;&amp;#x03BC;M), an agonist at CB1R, inhibits GABAergic synaptic transmission onto both superficial and deep medial entorhinal (mEC) neurones, but this has little effect on network oscillations in beta/gamma frequency bands. By contrast, the CB1R antagonist/inverse agonist LY320135 (500&amp;#x2009;nM), increased GABAergic synaptic activity and beta/gamma oscillatory activity in superficial mEC, was suppressed, whilst that in deep mEC was enhanced. These data indicate that cannabinoid-mediated effects on inhibitory synaptic activity may be constitutively active in vitro, and that modulation of CB1R activation using inverse agonists unmasks complex effects of CBR function on network activity. (Source: Neural Plasticity)</description>
            <author>Neural Plasticity</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2468844</comments>
            <pubDate>Wed, 10 Jun 2009 07:02:40 +0100</pubDate>
            <guid isPermaLink="false">2468844</guid>        </item>
        <item>
            <title>Antiaversive Effects of Cannabinoids: Is the Periaqueductal Gray Involved?</title>
            <link>http://www.medworm.com/index.php?rid=2468843&amp;cid=s_36794_168_f&amp;fid=37050&amp;url=http%3A%2F%2Fwww.hindawi.com%2Fjournals%2Fnp%2F2009%2F625469.html</link>
            <description>Cannabinoids play an important role in activity-dependent changes in synaptic activity and can interfere in several brain functions, including responses to aversive stimuli. The regions responsible for their effects, however, are still unclear. Cannabinoid type 1 (CB1) receptors are widely distributed in the central nervous system and are present in the periaqueductal gray (PAG), a midbrain structure closely involved in responses related to aversive states. Accordingly, exposure to stressful stimuli increases endocannabinoid (eCB) levels in the PAG, and local administration of CB1 agonists or drugs that facilitate eCB-mediated neurotransmission produces antinociceptive and antiaversive effects. To investigate if these drugs would also interfere in animal models that are sensitive to anxiol...</description>
            <author>Neural Plasticity</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2468843</comments>
            <pubDate>Wed, 10 Jun 2009 07:02:40 +0100</pubDate>
            <guid isPermaLink="false">2468843</guid>        </item>
        <item>
            <title>Progesterone Withdrawal-Evoked Plasticity of Neural Function in the Female Periaqueductal Grey 
Matter</title>
            <link>http://www.medworm.com/index.php?rid=2468842&amp;cid=s_36794_168_f&amp;fid=37050&amp;url=http%3A%2F%2Fwww.hindawi.com%2Fjournals%2Fnp%2F2009%2F730902.html</link>
            <description>Cyclical changes in production of neuroactive steroids during the oestrous cycle induce significant changes in 
GABAA receptor expression in female rats. In the periaqueductal grey (PAG) matter, upregulation of &amp;#x03B1;4&amp;#x03B2;1&amp;#x03B4; GABAA receptors occurs as progesterone levels fall during late dioestrus (LD) or during withdrawal from an exogenous progesterone dosing regime. The new receptors are likely to be extrasynaptically located on the GABAergic interneurone population and to mediate tonic currents. Electrophysiological studies showed that when &amp;#x03B1;4&amp;#x03B2;1&amp;#x03B4; GABAA receptor expression was increased, the excitability of the output neurones in the PAG increased, due to a decrease in the level of ongoing inhibitory tone from the GABAergic interneurones. The functional c...</description>
            <author>Neural Plasticity</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2468842</comments>
            <pubDate>Wed, 10 Jun 2009 07:02:40 +0100</pubDate>
            <guid isPermaLink="false">2468842</guid>        </item>
        <item>
            <title>Neuronal Plasticity in the Entorhinal Cortex</title>
            <link>http://www.medworm.com/index.php?rid=2468841&amp;cid=s_36794_168_f&amp;fid=37050&amp;url=http%3A%2F%2Fwww.hindawi.com%2Fjournals%2Fnp%2F2008%2F314785.html</link>
            <description>(Source: Neural Plasticity)</description>
            <author>Neural Plasticity</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2468841</comments>
            <pubDate>Wed, 10 Jun 2009 07:02:40 +0100</pubDate>
            <guid isPermaLink="false">2468841</guid>        </item>
        <item>
            <title>Object-Place Recognition Learning Triggers Rapid Induction of Plasticity-Related Immediate Early Genes and Synaptic Proteins in the Rat Dentate Gyrus</title>
            <link>http://www.medworm.com/index.php?rid=2468840&amp;cid=s_36794_168_f&amp;fid=37050&amp;url=http%3A%2F%2Fwww.hindawi.com%2Fjournals%2Fnp%2F2008%2F269097.html</link>
            <description>Long-term recognition memory requires protein synthesis, but little is known about the coordinate regulation of specific genes. Here, we examined expression of the plasticity-associated immediate early genes (Arc, Zif268, and Narp) in the dentate gyrus following long-term object-place recognition learning in rats. RT-PCR analysis from dentate gyrus tissue collected shortly after training did not reveal learning-specific changes in Arc mRNA expression. In situ hybridization and immunohistochemistry were therefore used to assess possible sparse effects on gene expression. Learning about objects increased the density of granule cells expressing Arc, and to a lesser extent Narp, specifically in the dorsal blade of the dentate gyrus, while Zif268 expression was elevated across both blades. Thus...</description>
            <author>Neural Plasticity</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2468840</comments>
            <pubDate>Wed, 10 Jun 2009 07:02:40 +0100</pubDate>
            <guid isPermaLink="false">2468840</guid>        </item>
        <item>
            <title>The Role of the Periaqueductal Gray in the Modulation of Pain in Males and Females: Are the Anatomy and Physiology Really that Different?</title>
            <link>http://www.medworm.com/index.php?rid=2468839&amp;cid=s_36794_168_f&amp;fid=37050&amp;url=http%3A%2F%2Fwww.hindawi.com%2Fjournals%2Fnp%2F2009%2F462879.html</link>
            <description>Anatomical and physiological studies conducted in the 1960s identified the periaqueductal gray (PAG) and its descending projections to the rostral ventromedial medulla (RVM) and spinal cord dorsal horn, as a primary anatomical pathway mediating opioid-based analgesia. Since these initial studies, the PAG-RVM-spinal cord pathway has been characterized anatomically and physiologically in a wide range of vertebrate species. Remarkably, the majority of these studies were conducted exclusively in males with the implicit assumption that the anatomy and physiology of this circuit were the same in females; however, this is not the case. It is well established that morphine administration produces greater antinociception in males compared to females. Recent studies indicate that the PAG-RVM pathway...</description>
            <author>Neural Plasticity</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2468839</comments>
            <pubDate>Wed, 10 Jun 2009 07:02:40 +0100</pubDate>
            <guid isPermaLink="false">2468839</guid>        </item>
        <item>
            <title>Behavioral Consequences of Delta-Opioid Receptor Activation in the Periaqueductal Gray of Morphine Tolerant Rats</title>
            <link>http://www.medworm.com/index.php?rid=2468838&amp;cid=s_36794_168_f&amp;fid=37050&amp;url=http%3A%2F%2Fwww.hindawi.com%2Fjournals%2Fnp%2F2009%2F516328.html</link>
            <description>Chronic morphine administration shifts delta-opioid receptors (DORs) from the cytoplasm to the plasma membrane. Given that microinjection of morphine into the PAG produces antinociception, it is hypothesized that the movement of DORs to the membrane will allow antinociception to the DOR agonist deltorphin II as a way to compensate for morphine tolerance. Tolerance was induced by twice daily injections of morphine (5, 10, or 20&amp;#x2009;mg/kg, subcutaneous) for 3.5 days. Microinjection of deltorphin into the vPAG 6 hours after the last morphine injection produced a mild antinociception that did not vary in a consistent manner across morphine pretreatment doses or nociceptive tests. In contrast, deltorphin caused a decrease in activity in morphine tolerant rats that was associated with lying i...</description>
            <author>Neural Plasticity</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2468838</comments>
            <pubDate>Wed, 10 Jun 2009 07:02:40 +0100</pubDate>
            <guid isPermaLink="false">2468838</guid>        </item>
        <item>
            <title>Panic Disorder: Is the PAG Involved?</title>
            <link>http://www.medworm.com/index.php?rid=2468837&amp;cid=s_36794_168_f&amp;fid=37050&amp;url=http%3A%2F%2Fwww.hindawi.com%2Fjournals%2Fnp%2F2009%2F108135.html</link>
            <description>Data from studies with humans have suggested that abnormalities of midbrain structures, including the periaqueductal gray matter (PAG), could be involved in the neurobiology of panic disorder (PD). The electrical stimulation of the PAG in neurosurgical patients induces panic-like symptoms and the effect of drugs that are effective in the treatment of PD in the simulation of public speaking model of anxiety is in agreement with data from animal models of PD. Structural neuroimaging studies have shown increases in gray matter volume of midbrain and pons of PD patients. There is also evidence of lower serotonin transporter and receptor binding, and increases of metabolism in the midbrain of PD patients. Nevertheless, these midbrain abnormalities can not be considered as specific findings, sin...</description>
            <author>Neural Plasticity</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2468837</comments>
            <pubDate>Wed, 10 Jun 2009 07:02:40 +0100</pubDate>
            <guid isPermaLink="false">2468837</guid>        </item>
        <item>
            <title>Afferent Connections to the Rostrolateral Part of the Periaqueductal Gray: A Critical Region Influencing the Motivation Drive to Hunt and Forage</title>
            <link>http://www.medworm.com/index.php?rid=2468836&amp;cid=s_36794_168_f&amp;fid=37050&amp;url=http%3A%2F%2Fwww.hindawi.com%2Fjournals%2Fnp%2F2009%2F612698.html</link>
            <description>Previous studies have shown that a particular site in the periaqueductal gray (PAG), the rostrolateral PAG, influences the motivation drive to forage or hunt. To have a deeper understanding on the putative paths involved in the decision-making process between foraging, hunting, and other behavioral responses, in the present investigation, we carried out a systematic analysis of the neural inputs to the rostrolateral PAG (rlPAG), using Fluorogold as a retrograde tracer. According to the present findings, the rlPAG appears to be importantly driven by medial prefrontal cortical areas involved in controlling attention-related and decision-making processes. Moreover, the rlPAG also receives a wealth of information from different amygdalar, hypothalamic, and brainstem sites related to feeding, d...</description>
            <author>Neural Plasticity</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2468836</comments>
            <pubDate>Wed, 10 Jun 2009 07:02:40 +0100</pubDate>
            <guid isPermaLink="false">2468836</guid>        </item>
        <item>
            <title>Viral Vector Induction of CREB Expression in the Periaqueductal Gray Induces a Predator Stress-Like Pattern of Changes in pCREB Expression, Neuroplasticity, and Anxiety in Rodents</title>
            <link>http://www.medworm.com/index.php?rid=2468835&amp;cid=s_36794_168_f&amp;fid=37050&amp;url=http%3A%2F%2Fwww.hindawi.com%2Fjournals%2Fnp%2F2009%2F904568.html</link>
            <description>Predator stress is lastingly anxiogenic. Phosphorylation of CREB to pCREB (phosphorylated cyclic AMP response element binding protein) is increased after predator stress in fear circuitry, including in the right lateral column of the PAG (periaqueductal gray). Predator stress also potentiates right but not left CeA-PAG (central amygdala-PAG) transmission up to 12 days after stress. The present study explored the functional significance of pCREB changes by increasing CREB expression in non-predator stressed rats through viral vectoring, and assessing the behavioral, electrophysiological and pCREB expression changes in comparison with handled and predator stressed controls. Increasing CREB expression in right PAG was anxiogenic in the elevated plus maze, had no effect on risk assessment, and...</description>
            <author>Neural Plasticity</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2468835</comments>
            <pubDate>Wed, 10 Jun 2009 07:02:40 +0100</pubDate>
            <guid isPermaLink="false">2468835</guid>        </item>
        <item>
            <title>The Periaqueductal Gray (PAG)</title>
            <link>http://www.medworm.com/index.php?rid=2468834&amp;cid=s_36794_168_f&amp;fid=37050&amp;url=http%3A%2F%2Fwww.hindawi.com%2Fjournals%2Fnp%2F2009%2F360907.html</link>
            <description>(Source: Neural Plasticity)</description>
            <author>Neural Plasticity</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2468834</comments>
            <pubDate>Wed, 10 Jun 2009 07:02:40 +0100</pubDate>
            <guid isPermaLink="false">2468834</guid>        </item>
        <item>
            <title>Auditory Stimulation Dishabituates Olfactory Responses via Noradrenergic Cortical Modulation</title>
            <link>http://www.medworm.com/index.php?rid=2468833&amp;cid=s_36794_168_f&amp;fid=37050&amp;url=http%3A%2F%2Fwww.hindawi.com%2Fjournals%2Fnp%2F2009%2F754014.html</link>
            <description>Dishabituation is a return of a habituated response if context or contingency changes. In the mammalian olfactory system, metabotropic glutamate receptor mediated synaptic depression of cortical afferents underlies short-term habituation to odors. It was hypothesized that a known antagonistic interaction between these receptors and norepinephrine &amp;#x00df;-receptors provides a mechanism for dishabituation. The results demonstrate that a 
         108&amp;#x2009;dB siren induces a two-fold increase in norepinephrine content in the piriform cortex. 
         The same auditory stimulus induces dishabituation of odor-evoked heart rate orienting bradycardia 
         responses in awake rats. Finally, blockade of piriform cortical norepinephrine &amp;#x00df;-receptors with bilateral intracortical infusio...</description>
            <author>Neural Plasticity</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2468833</comments>
            <pubDate>Wed, 10 Jun 2009 07:02:40 +0100</pubDate>
            <guid isPermaLink="false">2468833</guid>        </item>
        <item>
            <title>Visual Deprivation Decreases Somatic GAD65 Puncta Number on Layer 2/3 Pyramidal Neurons in Mouse Visual Cortex</title>
            <link>http://www.medworm.com/index.php?rid=2468832&amp;cid=s_36794_168_f&amp;fid=37050&amp;url=http%3A%2F%2Fwww.hindawi.com%2Fjournals%2Fnp%2F2009%2F415135.html</link>
            <description>Proper functioning of the visual system depends on maturation of both excitatory and inhibitory synapses within the visual cortex. Considering that perisomatic inhibition is one of the key factors that control the critical period in visual cortex, it is pertinent to understand its regulation by visual experience. To do this, we developed an immunohistochemical method that allows three-dimensional (3D) analysis of the glutamic acid decarboxylase (GAD) 65-positive inhibitory terminals in the visual cortex. Using this method on transgenic mice expressing yellow fluorescence protein (YFP) in a subset of neurons, we found that the number of somatic GAD65-puncta on individual layer 2/3 pyramidal neurons is reduced when mice are dark-reared from birth and reverted to normal levels by re-exposure ...</description>
            <author>Neural Plasticity</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2468832</comments>
            <pubDate>Wed, 10 Jun 2009 07:02:40 +0100</pubDate>
            <guid isPermaLink="false">2468832</guid>        </item>
        <item>
            <title>Afferent connections to the rostrolateral part of the periaqueductal gray: a critical region influencing the motivation drive to hunt and forage.</title>
            <link>http://www.medworm.com/index.php?rid=2310941&amp;cid=s_36794_25_f&amp;fid=36794&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19325910%26dopt%3DAbstract</link>
            <description>Authors: Mota-Ortiz SR, Sukikara MH, Felicio LF, Canteras NS
    Previous studies have shown that a particular site in the periaqueductal gray (PAG), the rostrolateral PAG, influences the motivation drive to forage or hunt. To have a deeper understanding on the putative paths involved in the decision-making process between foraging, hunting, and other behavioral responses, in the present investigation, we carried out a systematic analysis of the neural inputs to the rostrolateral PAG (rlPAG), using Fluorogold as a retrograde tracer. According to the present findings, the rlPAG appears to be importantly driven by medial prefrontal cortical areas involved in controlling attention-related and decision-making processes. Moreover, the rlPAG also receives a wealth of information from different a...</description>
            <author>Neural Plasticity</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2310941</comments>
            <pubDate>Wed, 08 Apr 2009 16:10:24 +0100</pubDate>
            <guid isPermaLink="false">2310941</guid>        </item>
        <item>
            <title>Auditory stimulation dishabituates olfactory responses via noradrenergic cortical modulation.</title>
            <link>http://www.medworm.com/index.php?rid=2310934&amp;cid=s_36794_25_f&amp;fid=36794&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19343110%26dopt%3DAbstract</link>
            <description>Authors: Smith JJ, Shionoya K, Sullivan RM, Wilson DA
    Dishabituation is a return of a habituated response if context or contingency changes. In the mammalian olfactory system, metabotropic glutamate receptor mediated synaptic depression of cortical afferents underlies short-term habituation to odors. It was hypothesized that a known antagonistic interaction between these receptors and norepinephrine ss-receptors provides a mechanism for dishabituation. The results demonstrate that a 108 dB siren induces a two-fold increase in norepinephrine content in the piriform cortex. The same auditory stimulus induces dishabituation of odor-evoked heart rate orienting bradycardia responses in awake rats. Finally, blockade of piriform cortical norepinephrine ss-receptors with bilateral intracortica...</description>
            <author>Neural Plasticity</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2310934</comments>
            <pubDate>Wed, 08 Apr 2009 16:10:24 +0100</pubDate>
            <guid isPermaLink="false">2310934</guid>        </item>
        <item>
            <title>The Periaqueductal Gray (PAG).</title>
            <link>http://www.medworm.com/index.php?rid=2310930&amp;cid=s_36794_25_f&amp;fid=36794&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19343197%26dopt%3DAbstract</link>
            <description>Authors: Lovick TA, Adamec R
    
    PMID: 19343197 [PubMed - in process] (Source: Neural Plasticity)</description>
            <author>Neural Plasticity</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2310930</comments>
            <pubDate>Wed, 08 Apr 2009 16:10:24 +0100</pubDate>
            <guid isPermaLink="false">2310930</guid>        </item>
        <item>
            <title>Viral Vector Induction of CREB Expression in the Periaqueductal Gray Induces a Predator Stress-Like Pattern of Changes in pCREB Expression, Neuroplasticity, and Anxiety in Rodents</title>
            <link>http://www.medworm.com/index.php?rid=2300773&amp;cid=s_36794_168_f&amp;fid=37050&amp;url=http%3A%2F%2Fwww.hindawi.com%2FGetArticle.aspx%3Fdoi%3D10.1155%2F2009%2F904568</link>
            <description>Predator stress is lastingly anxiogenic. Phosphorylation of CREB to pCREB (phosphorylated cyclic AMP response element binding protein) is increased after predator stress in fear circuitry, including in the right lateral column of the PAG (periaqueductal gray). Predator stress also potentiates right but not left CeA-PAG (central amygdala-PAG) transmission up to 12 days after stress. The present study explored the functional significance of pCREB changes by increasing CREB expression in non-predator stressed rats through viral vectoring, and assessing the behavioral, electrophysiological and pCREB expression changes in comparison with handled and predator stressed controls. Increasing CREB expression in right PAG was anxiogenic in the elevated plus maze, had no effect on risk assessment, and...</description>
            <author>Neural Plasticity</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2300773</comments>
            <pubDate>Fri, 03 Apr 2009 06:03:48 +0100</pubDate>
            <guid isPermaLink="false">2300773</guid>        </item>
        <item>
            <title>The Periaqueductal Gray (PAG)</title>
            <link>http://www.medworm.com/index.php?rid=2300772&amp;cid=s_36794_168_f&amp;fid=37050&amp;url=http%3A%2F%2Fwww.hindawi.com%2FGetArticle.aspx%3Fdoi%3D10.1155%2F2009%2F360907</link>
            <description>(Source: Neural Plasticity)</description>
            <author>Neural Plasticity</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2300772</comments>
            <pubDate>Fri, 03 Apr 2009 06:03:48 +0100</pubDate>
            <guid isPermaLink="false">2300772</guid>        </item>
        <item>
            <title>Auditory Stimulation Dishabituates Olfactory Responses via Noradrenergic Cortical Modulation</title>
            <link>http://www.medworm.com/index.php?rid=2300771&amp;cid=s_36794_168_f&amp;fid=37050&amp;url=http%3A%2F%2Fwww.hindawi.com%2FGetArticle.aspx%3Fdoi%3D10.1155%2F2009%2F754014</link>
            <description>Dishabituation is a return of a habituated response if context or contingency changes. In the mammalian olfactory system, metabotropic glutamate receptor mediated synaptic depression of cortical afferents underlies short-term habituation to odors. It was hypothesized that a known antagonistic interaction between these receptors and norepinephrine &amp;#x00df;-receptors provides a mechanism for dishabituation. The results demonstrate that a 
         108&amp;#x2009;dB siren induces a two-fold increase in norepinephrine content in the piriform cortex. 
         The same auditory stimulus induces dishabituation of odor-evoked heart rate orienting bradycardia 
         responses in awake rats. Finally, blockade of piriform cortical norepinephrine &amp;#x00df;-receptors with bilateral intracortical infusio...</description>
            <author>Neural Plasticity</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2300771</comments>
            <pubDate>Fri, 03 Apr 2009 06:03:48 +0100</pubDate>
            <guid isPermaLink="false">2300771</guid>        </item>
        <item>
            <title>Afferent Connections to the Rostrolateral Part of the Periaqueductal Gray: A Critical Region Influencing the Motivation Drive to Hunt and Forage</title>
            <link>http://www.medworm.com/index.php?rid=2275010&amp;cid=s_36794_168_f&amp;fid=37050&amp;url=http%3A%2F%2Fwww.hindawi.com%2FGetArticle.aspx%3Fdoi%3D10.1155%2F2009%2F612698</link>
            <description>Previous studies have shown that a particular site in the periaqueductal gray (PAG), the rostrolateral PAG, influences the motivation drive to forage or hunt. To have a deeper understanding on the putative paths involved in the decision-making process between foraging, hunting, and other behavioral responses, in the present investigation, we carried out a systematic analysis of the neural inputs to the rostrolateral PAG (rlPAG), using Fluorogold as a retrograde tracer. According to the present findings, the rlPAG appears to be importantly driven by medial prefrontal cortical areas involved in controlling attention-related and decision-making processes. Moreover, the rlPAG also receives a wealth of information from different amygdalar, hypothalamic, and brainstem sites related to feeding, d...</description>
            <author>Neural Plasticity</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2275010</comments>
            <pubDate>Thu, 19 Mar 2009 18:55:52 +0100</pubDate>
            <guid isPermaLink="false">2275010</guid>        </item>
        <item>
            <title>Panic disorder: is the PAG involved?</title>
            <link>http://www.medworm.com/index.php?rid=2265007&amp;cid=s_36794_25_f&amp;fid=36794&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19283082%26dopt%3DAbstract</link>
            <description>Authors: Del-Ben CM, Graeff FG
    Data from studies with humans have suggested that abnormalities of midbrain structures, including the periaqueductal gray matter (PAG), could be involved in the neurobiology of panic disorder (PD). The electrical stimulation of the PAG in neurosurgical patients induces panic-like symptoms and the effect of drugs that are effective in the treatment of PD in the simulation of public speaking model of anxiety is in agreement with data from animal models of PD. Structural neuroimaging studies have shown increases in gray matter volume of midbrain and pons of PD patients. There is also evidence of lower serotonin transporter and receptor binding, and increases of metabolism in the midbrain of PD patients. Nevertheless, these midbrain abnormalities can not be c...</description>
            <author>Neural Plasticity</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2265007</comments>
            <pubDate>Sun, 15 Mar 2009 06:51:25 +0100</pubDate>
            <guid isPermaLink="false">2265007</guid>        </item>
        <item>
            <title>Panic Disorder: Is the PAG Involved?</title>
            <link>http://www.medworm.com/index.php?rid=2261105&amp;cid=s_36794_168_f&amp;fid=37050&amp;url=http%3A%2F%2Fwww.hindawi.com%2FGetArticle.aspx%3Fdoi%3D10.1155%2F2009%2F108135</link>
            <description>Data from studies with humans have suggested that abnormalities of midbrain structures, including the periaqueductal gray matter (PAG), could be involved in the neurobiology of panic disorder (PD). The electrical stimulation of the PAG in neurosurgical patients induces panic-like symptoms and the effect of drugs that are effective in the treatment of PD in the simulation of public speaking model of anxiety is in agreement with data from animal models of PD. Structural neuroimaging studies have shown increases in gray matter volume of midbrain and pons of PD patients. There is also evidence of lower serotonin transporter and receptor binding, and increases of metabolism in the midbrain of PD patients. Nevertheless, these midbrain abnormalities can not be considered as specific findings, sin...</description>
            <author>Neural Plasticity</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2261105</comments>
            <pubDate>Sat, 14 Mar 2009 14:08:03 +0100</pubDate>
            <guid isPermaLink="false">2261105</guid>        </item>
        <item>
            <title>Behavioral consequences of delta-opioid receptor activation in the periaqueductal gray of morphine tolerant rats.</title>
            <link>http://www.medworm.com/index.php?rid=2249817&amp;cid=s_36794_25_f&amp;fid=36794&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19266049%26dopt%3DAbstract</link>
            <description>Authors: Morgan MM, Ashley MD, Ingram SL, Christie MJ
    Chronic morphine administration shifts delta-opioid receptors (DORs) from the cytoplasm to the plasma membrane. Given that microinjection of morphine into the PAG produces antinociception, it is hypothesized that the movement of DORs to the membrane will allow antinociception to the DOR agonist deltorphin II as a way to compensate for morphine tolerance. Tolerance was induced by twice daily injections of morphine (5, 10, or 20 mg/kg, subcutaneous) for 3.5 days. Microinjection of deltorphin into the vPAG 6 hours after the last morphine injection produced a mild antinociception that did not vary in a consistent manner across morphine pretreatment doses or nociceptive tests. In contrast, deltorphin caused a decrease in activity in morp...</description>
            <author>Neural Plasticity</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2249817</comments>
            <pubDate>Mon, 09 Mar 2009 05:00:24 +0100</pubDate>
            <guid isPermaLink="false">2249817</guid>        </item>
        <item>
            <title>Behavioral Consequences of Delta-Opioid Receptor Activation in the Periaqueductal Gray of Morphine Tolerant Rats</title>
            <link>http://www.medworm.com/index.php?rid=2218036&amp;cid=s_36794_168_f&amp;fid=37050&amp;url=http%3A%2F%2Fwww.hindawi.com%2FGetArticle.aspx%3Fdoi%3D10.1155%2F2009%2F516328</link>
            <description>Chronic morphine administration shifts delta-opioid receptors (DORs) from the cytoplasm to the plasma membrane. Given that microinjection of morphine into the PAG produces antinociception, it is hypothesized that the movement of DORs to the membrane will allow antinociception to the DOR agonist deltorphin II as a way to compensate for morphine tolerance. Tolerance was induced by twice daily injections of morphine (5, 10, or 20&amp;#x2009;mg/kg, subcutaneous) for 3.5 days. Microinjection of deltorphin into the vPAG 6 hours after the last morphine injection produced a mild antinociception that did not vary in a consistent manner across morphine pretreatment doses or nociceptive tests. In contrast, deltorphin caused a decrease in activity in morphine tolerant rats that was associated with lying i...</description>
            <author>Neural Plasticity</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2218036</comments>
            <pubDate>Fri, 27 Feb 2009 04:50:21 +0100</pubDate>
            <guid isPermaLink="false">2218036</guid>        </item>
        <item>
            <title>The role of the periaqueductal gray in the modulation of pain in males and females: are the anatomy and physiology really that different?</title>
            <link>http://www.medworm.com/index.php?rid=2168441&amp;cid=s_36794_25_f&amp;fid=36794&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19197373%26dopt%3DAbstract</link>
            <description>Authors: Loyd DR, Murphy AZ
    Anatomical and physiological studies conducted in the 1960s identified the periaqueductal gray (PAG) and its descending projections to the rostral ventromedial medulla (RVM) and spinal cord dorsal horn, as a primary anatomical pathway mediating opioid-based analgesia. Since these initial studies, the PAG-RVM-spinal cord pathway has been characterized anatomically and physiologically in a wide range of vertebrate species. Remarkably, the majority of these studies were conducted exclusively in males with the implicit assumption that the anatomy and physiology of this circuit were the same in females; however, this is not the case. It is well established that morphine administration produces greater antinociception in males compared to females. Recent studies i...</description>
            <author>Neural Plasticity</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2168441</comments>
            <pubDate>Sun, 08 Feb 2009 20:48:19 +0100</pubDate>
            <guid isPermaLink="false">2168441</guid>        </item>
        <item>
            <title>The Role of the Periaqueductal Gray in the Modulation of Pain in Males and Females: Are the Anatomy and Physiology Really that Different?</title>
            <link>http://www.medworm.com/index.php?rid=2142073&amp;cid=s_36794_168_f&amp;fid=37050&amp;url=http%3A%2F%2Fwww.hindawi.com%2FGetArticle.aspx%3Fdoi%3D10.1155%2F2009%2F462879</link>
            <description>Anatomical and physiological studies conducted in the 1960s identified the periaqueductal gray (PAG) and its descending projections to the rostral ventromedial medulla (RVM) and spinal cord dorsal horn, as a primary anatomical pathway mediating opioid-based analgesia. Since these initial studies, the PAG-RVM-spinal cord pathway has been characterized anatomically and physiologically in a wide range of vertebrate species. Remarkably, the majority of these studies were conducted exclusively in males with the implicit assumption that the anatomy and physiology of this circuit were the same in females; however, this is not the case. It is well established that morphine administration produces greater antinociception in males compared to females. Recent studies indicate that the PAG-RVM pathway...</description>
            <author>Neural Plasticity</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2142073</comments>
            <pubDate>Thu, 29 Jan 2009 16:23:03 +0100</pubDate>
            <guid isPermaLink="false">2142073</guid>        </item>
        <item>
            <title>Object-Place Recognition Learning Triggers Rapid Induction of Plasticity-Related Immediate Early Genes and Synaptic Proteins in the Rat Dentate Gyrus</title>
            <link>http://www.medworm.com/index.php?rid=2132715&amp;cid=s_36794_168_f&amp;fid=37050&amp;url=http%3A%2F%2Fwww.hindawi.com%2FGetArticle.aspx%3Fdoi%3D10.1155%2F2008%2F269097</link>
            <description>Long-term recognition memory requires protein synthesis, but little is known about the coordinate regulation of specific genes. Here, we examined expression of the plasticity-associated immediate early genes (Arc, Zif268, and Narp) in the dentate gyrus following long-term object-place recognition learning in rats. RT-PCR analysis from dentate gyrus tissue collected shortly after training did not reveal learning-specific changes in Arc mRNA expression. In situ hybridization and immunohistochemistry were therefore used to assess possible sparse effects on gene expression. Learning about objects increased the density of granule cells expressing Arc, and to a lesser extent Narp, specifically in the dorsal blade of the dentate gyrus, while Zif268 expression was elevated across both blades. Thus...</description>
            <author>Neural Plasticity</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2132715</comments>
            <pubDate>Mon, 26 Jan 2009 12:11:48 +0100</pubDate>
            <guid isPermaLink="false">2132715</guid>        </item>
        <item>
            <title>Neuronal Plasticity in the Entorhinal Cortex</title>
            <link>http://www.medworm.com/index.php?rid=2075960&amp;cid=s_36794_168_f&amp;fid=37050&amp;url=http%3A%2F%2Fwww.hindawi.com%2FGetArticle.aspx%3Fdoi%3D10.1155%2F2008%2F314785</link>
            <description>(Source: Neural Plasticity)</description>
            <author>Neural Plasticity</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2075960</comments>
            <pubDate>Sat, 03 Jan 2009 17:25:27 +0100</pubDate>
            <guid isPermaLink="false">2075960</guid>        </item>
        <item>
            <title>Antiaversive effects of cannabinoids: is the periaqueductal gray involved?</title>
            <link>http://www.medworm.com/index.php?rid=2053908&amp;cid=s_36794_25_f&amp;fid=36794&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19096514%26dopt%3DAbstract</link>
            <description>Authors: Moreira FA, Aguiar DC, Campos AC, Lisboa SF, Terzian AL, Resstel LB, Guimar&amp;#xE3;es FS
    Cannabinoids play an important role in activity-dependent changes in synaptic activity and can interfere in several brain functions, including responses to aversive stimuli. The regions responsible for their effects, however, are still unclear. Cannabinoid type 1 (CB1) receptors are widely distributed in the central nervous system and are present in the periaqueductal gray (PAG), a midbrain structure closely involved in responses related to aversive states. Accordingly, exposure to stressful stimuli increases endocannabinoid (eCB) levels in the PAG, and local administration of CB1 agonists or drugs that facilitate eCB-mediated neurotransmission produces antinociceptive and antiaversive effec...</description>
            <author>Neural Plasticity</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2053908</comments>
            <pubDate>Sat, 20 Dec 2008 15:31:02 +0100</pubDate>
            <guid isPermaLink="false">2053908</guid>        </item>
        <item>
            <title>Progesterone withdrawal-evoked plasticity of neural function in the female periaqueductal grey matter.</title>
            <link>http://www.medworm.com/index.php?rid=2053907&amp;cid=s_36794_25_f&amp;fid=36794&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19096515%26dopt%3DAbstract</link>
            <description>Authors: Lovick TA, Devall AJ
    Cyclical changes in production of neuroactive steroids during the oestrous cycle induce significant changes in GABA(A) receptor expression in female rats. In the periaqueductal grey (PAG) matter, upregulation of alpha4beta1delta GABA(A) receptors occurs as progesterone levels fall during late dioestrus (LD) or during withdrawal from an exogenous progesterone dosing regime. The new receptors are likely to be extrasynaptically located on the GABAergic interneurone population and to mediate tonic currents. Electrophysiological studies showed that when alpha4beta1delta GABA(A) receptor expression was increased, the excitability of the output neurones in the PAG increased, due to a decrease in the level of ongoing inhibitory tone from the GABAergic interneurone...</description>
            <author>Neural Plasticity</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2053907</comments>
            <pubDate>Sat, 20 Dec 2008 15:30:51 +0100</pubDate>
            <guid isPermaLink="false">2053907</guid>        </item>
        <item>
            <title>Modulation of Network Oscillatory Activity and GABAergic Synaptic Transmission by CB1 Cannabinoid Receptors in the Rat Medial Entorhinal Cortex.</title>
            <link>http://www.medworm.com/index.php?rid=2041069&amp;cid=s_36794_25_f&amp;fid=36794&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19079598%26dopt%3DAbstract</link>
            <description>We report that arachidonylcyclopropylamide (ACPA; 10 muM), an agonist at CB1R, inhibits GABAergic synaptic transmission onto both superficial and deep medial entorhinal (mEC) neurones, but this has little effect on network oscillations in beta/gamma frequency bands. By contrast, the CB1R antagonist/inverse agonist LY320135 (500 nM), increased GABAergic synaptic activity and beta/gamma oscillatory activity in superficial mEC, was suppressed, whilst that in deep mEC was enhanced. These data indicate that cannabinoid-mediated effects on inhibitory synaptic activity may be constitutively active in vitro, and that modulation of CB1R activation using inverse agonists unmasks complex effects of CBR function on network activity.
    PMID: 19079598 [PubMed - in process] (Source: Neural Plasticity)</description>
            <author>Neural Plasticity</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2041069</comments>
            <pubDate>Wed, 17 Dec 2008 14:41:45 +0100</pubDate>
            <guid isPermaLink="false">2041069</guid>        </item>
        <item>
            <title>The role of GLU K5-containing kainate receptors in entorhinal cortex gamma frequency oscillations.</title>
            <link>http://www.medworm.com/index.php?rid=2022217&amp;cid=s_36794_25_f&amp;fid=36794&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19043593%26dopt%3DAbstract</link>
            <description>Authors: Stanger HL, Alford R, Jane DE, Cunningham MO
    Using in vitro brain slices of hippocampus and cortex, neuronal oscillations in the frequency range of 30-80 Hz (gamma frequency oscillations) can be induced by a number of pharmacological manipulations. The most routinely used is the bath application of the broad-spectrum glutamate receptor agonist, kainic acid. In the hippocampus, work using transgenic kainate receptor knockout mice have revealed information about the specific subunit composition of the kainate receptor implicated in the generation and maintenance of the gamma frequency oscillation. However, there is a paucity of such detail regarding gamma frequency oscillation in the cortex. Using specific pharmacological agonists and antagonists for the kainate receptor, we hav...</description>
            <author>Neural Plasticity</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2022217</comments>
            <pubDate>Tue, 09 Dec 2008 13:10:25 +0100</pubDate>
            <guid isPermaLink="false">2022217</guid>        </item>
        <item>
            <title>Antiaversive Effects of Cannabinoids: Is the Periaqueductal Gray Involved?</title>
            <link>http://www.medworm.com/index.php?rid=2007270&amp;cid=s_36794_168_f&amp;fid=37050&amp;url=http%3A%2F%2Fwww.hindawi.com%2FGetArticle.aspx%3Fdoi%3D10.1155%2F2009%2F625469</link>
            <description>Cannabinoids play an important role in activity-dependent changes in synaptic activity and can interfere in several brain functions, including responses to aversive stimuli. The regions responsible for their effects, however, are still unclear. Cannabinoid type 1 (CB1) receptors are widely distributed in the central nervous system and are present in the periaqueductal gray (PAG), a midbrain structure closely involved in responses related to aversive states. Accordingly, exposure to stressful stimuli increases endocannabinoid (eCB) levels in the PAG, and local administration of CB1 agonists or drugs that facilitate eCB-mediated neurotransmission produces antinociceptive and antiaversive effects. To investigate if these drugs would also interfere in animal models that are sensitive to anxiol...</description>
            <author>Neural Plasticity</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2007270</comments>
            <pubDate>Wed, 03 Dec 2008 15:17:11 +0100</pubDate>
            <guid isPermaLink="false">2007270</guid>        </item>
        <item>
            <title>Progesterone Withdrawal-Evoked Plasticity of Neural Function in the Female Periaqueductal Grey 
Matter</title>
            <link>http://www.medworm.com/index.php?rid=2007269&amp;cid=s_36794_168_f&amp;fid=37050&amp;url=http%3A%2F%2Fwww.hindawi.com%2FGetArticle.aspx%3Fdoi%3D10.1155%2F2009%2F730902</link>
            <description>Cyclical changes in production of neuroactive steroids during the oestrous cycle induce significant changes in 
GABAA receptor expression in female rats. In the periaqueductal grey (PAG) matter, upregulation of &amp;#x03B1;4&amp;#x03B2;1&amp;#x03B4; GABAA receptors occurs as progesterone levels fall during late dioestrus (LD) or during withdrawal from an exogenous progesterone dosing regime. The new receptors are likely to be extrasynaptically located on the GABAergic interneurone population and to mediate tonic currents. Electrophysiological studies showed that when &amp;#x03B1;4&amp;#x03B2;1&amp;#x03B4; GABAA receptor expression was increased, the excitability of the output neurones in the PAG increased, due to a decrease in the level of ongoing inhibitory tone from the GABAergic interneurones. The functional c...</description>
            <author>Neural Plasticity</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2007269</comments>
            <pubDate>Wed, 03 Dec 2008 15:17:11 +0100</pubDate>
            <guid isPermaLink="false">2007269</guid>        </item>
        <item>
            <title>The Role of GLU(K5)-Containing Kainate Receptors in Entorhinal Cortex Gamma Frequency Oscillations.</title>
            <link>http://www.medworm.com/index.php?rid=2007105&amp;cid=s_36794_25_f&amp;fid=36794&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19043593%26dopt%3DAbstract</link>
            <description>Authors: Stanger HL, Alford R, Jane DE, Cunningham MO
    Using in vitro brain slices of hippocampus and cortex, neuronal oscillations in the frequency range of 30-80 Hz (gamma frequency oscillations) can be induced by a number of pharmacological manipulations. The most routinely used is the bath application of the broad-spectrum glutamate receptor agonist, kainic acid. In the hippocampus, work using transgenic kainate receptor knockout mice have revealed information about the specific subunit composition of the kainate receptor implicated in the generation and maintenance of the gamma frequency oscillation. However, there is a paucity of such detail regarding gamma frequency oscillation in the cortex. Using specific pharmacological agonists and antagonists for the kainate receptor, we hav...</description>
            <author>Neural Plasticity</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2007105</comments>
            <pubDate>Wed, 03 Dec 2008 14:34:19 +0100</pubDate>
            <guid isPermaLink="false">2007105</guid>        </item>
        <item>
            <title>Modulation of Network Oscillatory Activity and GABAergic Synaptic Transmission by CB1 Cannabinoid Receptors in the Rat Medial Entorhinal Cortex</title>
            <link>http://www.medworm.com/index.php?rid=1999625&amp;cid=s_36794_168_f&amp;fid=37050&amp;url=http%3A%2F%2Fwww.hindawi.com%2FGetArticle.aspx%3Fdoi%3D10.1155%2F2008%2F808564</link>
            <description>We report that arachidonylcyclopropylamide (ACPA; 10&amp;#x2009;&amp;#x03BC;M), an agonist at CB1R, inhibits GABAergic synaptic transmission onto both superficial and deep medial entorhinal (mEC) neurones, but this has little effect on network oscillations in beta/gamma frequency bands. By contrast, the CB1R antagonist/inverse agonist LY320135 (500&amp;#x2009;nM), increased GABAergic synaptic activity and beta/gamma oscillatory activity in superficial mEC, was suppressed, whilst that in deep mEC was enhanced. These data indicate that cannabinoid-mediated effects on inhibitory synaptic activity may be constitutively active in vitro, and that modulation of CB1R activation using inverse agonists unmasks complex effects of CBR function on network activity. (Source: Neural Plasticity)</description>
            <author>Neural Plasticity</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1999625</comments>
            <pubDate>Mon, 01 Dec 2008 12:54:09 +0100</pubDate>
            <guid isPermaLink="false">1999625</guid>        </item>
        <item>
            <title>The Role of GLUK5-Containing Kainate Receptors in Entorhinal Cortex Gamma Frequency Oscillations</title>
            <link>http://www.medworm.com/index.php?rid=1970124&amp;cid=s_36794_168_f&amp;fid=37050&amp;url=http%3A%2F%2Fwww.hindawi.com%2FGetArticle.aspx%3Fdoi%3D10.1155%2F2008%2F401645</link>
            <description>Using in vitro brain slices of hippocampus and cortex, neuronal oscillations in the frequency range of 30&amp;#8211;80&amp;#x2009;Hz (gamma frequency oscillations) can be induced by a number of pharmacological manipulations. The most routinely used is the bath application of the broad-spectrum glutamate receptor agonist, kainic acid. In the hippocampus, work using transgenic kainate receptor knockout mice have revealed information about the specific subunit composition of the kainate receptor implicated in the generation and maintenance of the gamma frequency oscillation. However, there is a paucity of such detail regarding gamma frequency oscillation in the cortex. Using specific pharmacological agonists and antagonists for the kainate receptor, we have set out to examine the contribution of kain...</description>
            <author>Neural Plasticity</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1970124</comments>
            <pubDate>Wed, 19 Nov 2008 13:41:06 +0100</pubDate>
            <guid isPermaLink="false">1970124</guid>        </item>
        <item>
            <title>Understanding Stress-Related Behavioral Phenotypes: Report from the 1st International Neuroscience Summer School and the 11th International &amp;#8220;Stress and Behavior&amp;#8221; Conference</title>
            <link>http://www.medworm.com/index.php?rid=1970123&amp;cid=s_36794_168_f&amp;fid=37050&amp;url=http%3A%2F%2Fwww.hindawi.com%2FGetArticle.aspx%3Fdoi%3D10.1155%2F2008%2F543075</link>
            <description>The 1st International Neuroscience Summer School and the 11th International Multidisciplinary Neuroscience and Biopsychiatry Conference on Stress and Behavior were held in St. Petersburg, Russia, during May 9&amp;#8211;20, 2008. The summer school gathered 30 talented young scientists from 15 countries worldwide, and was dedicated to different topics of behavioral neuroscience. Many interactive courses were provided on neuropharmacology, animal phenotyping, and biopsychology. The conference&amp;#39;s excellent scientific and social program attracted almost 500 delegates from 40 countries from many areas of stress research. The eclectic interaction between medical doctors, basic scientists, psychologists, and students made for a productive and collaborative environment, which contributed greatly to ...</description>
            <author>Neural Plasticity</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1970123</comments>
            <pubDate>Wed, 19 Nov 2008 13:41:06 +0100</pubDate>
            <guid isPermaLink="false">1970123</guid>        </item>
        <item>
            <title>The role of NMDA receptor subtypes in short-term plasticity in the rat entorhinal cortex.</title>
            <link>http://www.medworm.com/index.php?rid=1943904&amp;cid=s_36794_25_f&amp;fid=36794&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D18989370%26dopt%3DAbstract</link>
            <description>Authors: Chamberlain SE, Yang J, Jones RS
    We have previously shown that spontaneous release of glutamate in the entorhinal cortex (EC) is tonically facilitated via activation of presynaptic NMDA receptors (NMDAr) containing the NR2B subunit. Here we show that the same receptors mediate short-term plasticity manifested by frequency-dependent facilitation of evoked glutamate release at these synapses. Whole-cell patch-clamp recordings were made from layer V pyramidal neurones in rat EC slices. Evoked excitatory postsynaptic currents showed strong facilitation at relatively low frequencies (3 Hz) of activation. Facilitation was abolished by an NR2B-selective blocker (Ro 25-6981), but unaffected by NR2A-selective antagonists (Zn(2+), NVP-AAM077). In contrast, postsynaptic NMDAr-mediated re...</description>
            <author>Neural Plasticity</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1943904</comments>
            <pubDate>Sat, 08 Nov 2008 14:54:06 +0100</pubDate>
            <guid isPermaLink="false">1943904</guid>        </item>
        <item>
            <title>The Role of NMDA Receptor Subtypes in Short-Term Plasticity in the Rat Entorhinal Cortex</title>
            <link>http://www.medworm.com/index.php?rid=1915513&amp;cid=s_36794_168_f&amp;fid=37050&amp;url=http%3A%2F%2Fwww.hindawi.com%2FGetArticle.aspx%3Fdoi%3D10.1155%2F2008%2F872456</link>
            <description>We have previously shown that spontaneous release of glutamate in the entorhinal cortex (EC) is tonically facilitated via activation of presynaptic NMDA receptors 
 (NMDAr) containing the NR2B subunit. Here we show that the same receptors mediate short-term plasticity manifested by frequency-dependent facilitation of evoked glutamate release at these synapses. Whole-cell patch-clamp recordings were made from layer V pyramidal neurones in rat EC slices. Evoked excitatory postsynaptic currents showed strong facilitation at relatively low frequencies (3&amp;#x2009;Hz) of activation. Facilitation was abolished by an NR2B-selective blocker (Ro 25-6981), but unaffected by NR2A-selective antagonists (Zn2+, NVP-AAM077). In contrast, postsynaptic NMDAr-mediated responses could be reduced by subunit-sel...</description>
            <author>Neural Plasticity</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1915513</comments>
            <pubDate>Wed, 29 Oct 2008 16:14:33 +0100</pubDate>
            <guid isPermaLink="false">1915513</guid>        </item>
        <item>
            <title>Dopaminergic suppression of synaptic transmission in the lateral entorhinal cortex.</title>
            <link>http://www.medworm.com/index.php?rid=1764669&amp;cid=s_36794_25_f&amp;fid=36794&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D18769495%26dopt%3DAbstract</link>
            <description>Authors: Caruana DA, Chapman CA
    Dopaminergic projections to the superficial layers of the lateral entorhinal cortex can modulate the strength of olfactory inputs to the region. We have found that low concentrations of dopamine facilitate field EPSPs in the entorhinal cortex, and that higher concentrations of dopamine suppress synaptic responses. Here, we have used whole-cell current clamp recordings from layer II neurons to determine the mechanisms of the suppression. Dopamine (10 to 50 muM) hyperpolarized membrane potential and reversibly suppressed the amplitude of EPSPs evoked by layer I stimulation. Both AMPA- and NMDA-mediated components were suppressed, and paired-pulse facilitation was also enhanced indicating that the suppression is mediated largely by reduced glutamate release...</description>
            <author>Neural Plasticity</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1764669</comments>
            <pubDate>Fri, 05 Sep 2008 14:15:27 +0100</pubDate>
            <guid isPermaLink="false">1764669</guid>        </item>
        <item>
            <title>What does the anatomical organization of the entorhinal cortex tell us?</title>
            <link>http://www.medworm.com/index.php?rid=1764668&amp;cid=s_36794_25_f&amp;fid=36794&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D18769556%26dopt%3DAbstract</link>
            <description>Authors: Canto CB, Wouterlood FG, Witter MP
    The entorhinal cortex is commonly perceived as a major input and output structure of the hippocampal formation, entertaining the role of the nodal point of cortico-hippocampal circuits. Superficial layers receive convergent cortical information, which is relayed to structures in the hippocampus, and hippocampal output reaches deep layers of entorhinal cortex, that project back to the cortex. The finding of the grid cells in all layers and reports on interactions between deep and superficial layers indicate that this rather simplistic perception may be at fault. Therefore, an integrative approach on the entorhinal cortex, that takes into account recent additions to our knowledge database on entorhinal connectivity, is timely. We argue that lay...</description>
            <author>Neural Plasticity</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1764668</comments>
            <pubDate>Fri, 05 Sep 2008 14:15:27 +0100</pubDate>
            <guid isPermaLink="false">1764668</guid>        </item>
        <item>
            <title>What Does the Anatomical Organization of the Entorhinal Cortex Tell Us?</title>
            <link>http://www.medworm.com/index.php?rid=1740068&amp;cid=s_36794_168_f&amp;fid=37050&amp;url=http%3A%2F%2Fwww.hindawi.com%2FGetArticle.aspx%3Fdoi%3D10.1155%2F2008%2F381243</link>
            <description>The entorhinal cortex is commonly perceived as a major input and output structure of the hippocampal formation, entertaining the role of the nodal point of cortico-hippocampal circuits. Superficial layers receive convergent cortical information, which is relayed to structures in the hippocampus, and hippocampal output reaches deep layers of entorhinal cortex, that project back to the cortex. The finding of the grid cells in all layers and reports on interactions between deep and superficial layers  indicate that this rather simplistic perception may be at fault. Therefore, an integrative approach on the entorhinal cortex, that takes into account recent additions to our knowledge database on entorhinal connectivity, is timely. We argue that layers in entorhinal cortex show different functio...</description>
            <author>Neural Plasticity</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1740068</comments>
            <pubDate>Fri, 29 Aug 2008 13:36:46 +0100</pubDate>
            <guid isPermaLink="false">1740068</guid>        </item>
        <item>
            <title>Dopaminergic Suppression of Synaptic Transmission in the Lateral Entorhinal Cortex</title>
            <link>http://www.medworm.com/index.php?rid=1730883&amp;cid=s_36794_168_f&amp;fid=37050&amp;url=http%3A%2F%2Fwww.hindawi.com%2FGetArticle.aspx%3Fdoi%3D10.1155%2F2008%2F203514</link>
            <description>Dopaminergic projections to the superficial layers of the lateral entorhinal cortex can modulate the strength of olfactory inputs to the region. We have found that low concentrations of dopamine facilitate field EPSPs in the entorhinal cortex, and that higher concentrations of dopamine suppress synaptic responses. Here, we have used whole-cell current clamp recordings from layer II neurons to determine the mechanisms of the suppression. Dopamine (10 to 50&amp;#x2009;&amp;#x03BC;M)
hyperpolarized membrane potential and reversibly suppressed the amplitude of EPSPs evoked by layer I stimulation. Both AMPA- and NMDA-mediated components were suppressed, and paired-pulse facilitation was also enhanced indicating that the suppression is mediated largely by reduced glutamate release. Blockade of D2-like r...</description>
            <author>Neural Plasticity</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1730883</comments>
            <pubDate>Mon, 25 Aug 2008 14:26:01 +0100</pubDate>
            <guid isPermaLink="false">1730883</guid>        </item>
        <item>
            <title>Postsynaptic signals mediating induction of long-term synaptic depression in the entorhinal cortex.</title>
            <link>http://www.medworm.com/index.php?rid=1675618&amp;cid=s_36794_25_f&amp;fid=36794&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D18670611%26dopt%3DAbstract</link>
            <description>Authors: Kourrich S, Glasgow SD, Caruana DA, Chapman CA
    The entorhinal cortex receives a large projection from the piriform cortex, and synaptic plasticity in this pathway may affect olfactory processing. In vitro whole cell recordings have been used here to investigate postsynaptic signalling mechanisms that mediate the induction of long-term synaptic depression (LTD) in layer II entorhinal cortex cells. To induce LTD, pairs of pulses, using a 30-millisecond interval, were delivered at 1 Hz for 15 minutes. Induction of LTD was blocked by the NMDA receptor antagonist APV and by the calcium chelator BAPTA, consistent with a requirement for calcium influx via NMDA receptors. Induction of LTD was blocked when the FK506 was included in the intracellular solution to block the phosphatase ca...</description>
            <author>Neural Plasticity</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1675618</comments>
            <pubDate>Sat, 02 Aug 2008 17:28:18 +0100</pubDate>
            <guid isPermaLink="false">1675618</guid>        </item>
        <item>
            <title>Linking cellular mechanisms to behavior: entorhinal persistent spiking and membrane potential oscillations may underlie path integration, grid cell firing, and episodic memory.</title>
            <link>http://www.medworm.com/index.php?rid=1675617&amp;cid=s_36794_25_f&amp;fid=36794&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D18670635%26dopt%3DAbstract</link>
            <description>This article reviews physiological data on persistent spiking and membrane potential oscillations in entorhinal cortex then presents models showing how both these cellular mechanisms could contribute to properties observed during unit recording, including grid cell firing, and how they could underlie behavioural functions including path integration. The interaction of oscillations and persistent firing could contribute to encoding and retrieval of trajectories through space and time as a mechanism relevant to episodic memory.
    PMID: 18670635 [PubMed - in process] (Source: Neural Plasticity)</description>
            <author>Neural Plasticity</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1675617</comments>
            <pubDate>Sat, 02 Aug 2008 17:28:18 +0100</pubDate>
            <guid isPermaLink="false">1675617</guid>        </item>
        <item>
            <title>Spontaneous plasticity of multineuronal activity patterns in activated hippocampal networks.</title>
            <link>http://www.medworm.com/index.php?rid=1646778&amp;cid=s_36794_25_f&amp;fid=36794&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D18645610%26dopt%3DAbstract</link>
            <description>Authors: Usami A, Matsuki N, Ikegaya Y
    Using functional multineuron imaging with single-cell resolution, we examined how hippocampal networks by themselves change the spatiotemporal patterns of spontaneous activity during the course of emitting spontaneous activity. When extracellular ionic concentrations were changed to those that mimicked in vivo conditions, spontaneous activity was increased in active cell number and activity frequency. When ionic compositions were restored to the control conditions, the activity level returned to baseline, but the weighted spatial dispersion of active cells, as assessed by entropy-based metrics, did not. Thus, the networks can modify themselves by altering the internal structure of their correlated activity, even though they as a whole maintained t...</description>
            <author>Neural Plasticity</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1646778</comments>
            <pubDate>Wed, 23 Jul 2008 13:49:58 +0100</pubDate>
            <guid isPermaLink="false">1646778</guid>        </item>
        <item>
            <title>Postsynaptic Signals Mediating Induction of Long-Term Synaptic Depression in the Entorhinal Cortex</title>
            <link>http://www.medworm.com/index.php?rid=1643151&amp;cid=s_36794_168_f&amp;fid=37050&amp;url=http%3A%2F%2Fwww.hindawi.com%2FGetArticle.aspx%3Fdoi%3D10.1155%2F2008%2F840374</link>
            <description>The entorhinal cortex receives a large projection from the piriform cortex, and synaptic plasticity in this pathway may affect olfactory processing. In vitro whole cell recordings have been used here to investigate postsynaptic signalling mechanisms that mediate the induction of long-term synaptic depression (LTD) in layer II entorhinal cortex cells. To induce LTD, pairs of pulses, using a 30-millisecond interval, were delivered at 1&amp;#x2009;Hz for 15&amp;#x2009;minutes. Induction of LTD was blocked by the NMDA receptor antagonist APV and by the calcium chelator BAPTA, consistent with a requirement for calcium influx via NMDA receptors. Induction of LTD was blocked when the FK506 was included in the intracellular solution to block the phosphatase calcineurin. Okadaic acid, which blocks activati...</description>
            <author>Neural Plasticity</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1643151</comments>
            <pubDate>Tue, 22 Jul 2008 14:56:01 +0100</pubDate>
            <guid isPermaLink="false">1643151</guid>        </item>
        <item>
            <title>Linking Cellular Mechanisms to Behavior: Entorhinal Persistent Spiking and Membrane Potential Oscillations May Underlie Path Integration, Grid Cell Firing, and Episodic Memory</title>
            <link>http://www.medworm.com/index.php?rid=1640546&amp;cid=s_36794_168_f&amp;fid=37050&amp;url=http%3A%2F%2Fwww.hindawi.com%2FGetArticle.aspx%3Fdoi%3D10.1155%2F2008%2F658323</link>
            <description>This article reviews physiological data on persistent spiking and membrane potential oscillations in entorhinal cortex then presents models showing how both these cellular mechanisms could contribute to properties observed during unit recording, including grid cell firing, and how they could underlie behavioural functions including path integration. The interaction of oscillations and persistent firing could contribute to encoding and retrieval of trajectories through space and time as a mechanism relevant to episodic memory. (Source: Neural Plasticity)</description>
            <author>Neural Plasticity</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1640546</comments>
            <pubDate>Mon, 21 Jul 2008 15:51:14 +0100</pubDate>
            <guid isPermaLink="false">1640546</guid>        </item>
        <item>
            <title>Spontaneous Plasticity of Multineuronal Activity Patterns in Activated Hippocampal Networks</title>
            <link>http://www.medworm.com/index.php?rid=1618339&amp;cid=s_36794_168_f&amp;fid=37050&amp;url=http%3A%2F%2Fwww.hindawi.com%2FGetArticle.aspx%3Fdoi%3D10.1155%2F2008%2F108969</link>
            <description>Using functional multineuron imaging with single-cell resolution, we examined how hippocampal networks by themselves change the spatiotemporal patterns of spontaneous activity during the course of emitting spontaneous activity. When extracellular ionic concentrations were changed to those that mimicked in vivo conditions, spontaneous activity was increased in active cell number and activity frequency. When ionic compositions were restored to the control conditions, the activity level returned to baseline, but the weighted spatial dispersion of active cells, as assessed by entropy-based metrics, did not. Thus, the networks can modify themselves by altering the internal structure of their correlated activity, even though they as a whole maintained the same level of activity in space and time...</description>
            <author>Neural Plasticity</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1618339</comments>
            <pubDate>Mon, 14 Jul 2008 13:41:52 +0100</pubDate>
            <guid isPermaLink="false">1618339</guid>        </item>
        <item>
            <title>Complementary roles of hippocampus and medial entorhinal cortex in episodic memory.</title>
            <link>http://www.medworm.com/index.php?rid=1606933&amp;cid=s_36794_25_f&amp;fid=36794&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D18615199%26dopt%3DAbstract</link>
            <description>Authors: Lipton PA, Eichenbaum H
    Spatial mapping and navigation are figured prominently in the extant literature that describes hippocampal function. The medial entorhinal cortex is likewise attracting increasing interest, insofar as evidence accumulates that this area also contributes to spatial information processing. Here, we discuss recent electrophysiological findings that offer an alternate view of hippocampal and medial entorhinal function. These findings suggest complementary contributions of the hippocampus and medial entorhinal cortex in support of episodic memory, wherein hippocampal networks encode sequences of events that compose temporally and spatially extended episodes, whereas medial entorhinal networks disambiguate overlapping episodes by binding sequential events int...</description>
            <author>Neural Plasticity</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1606933</comments>
            <pubDate>Fri, 11 Jul 2008 14:31:04 +0100</pubDate>
            <guid isPermaLink="false">1606933</guid>        </item>
        <item>
            <title>Effect of prenatal protein malnutrition on long-term potentiation and BDNF protein expression in the rat entorhinal cortex after neocortical and hippocampal tetanization.</title>
            <link>http://www.medworm.com/index.php?rid=1597337&amp;cid=s_36794_25_f&amp;fid=36794&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D18604298%26dopt%3DAbstract</link>
            <description>Authors: Hern&amp;#xE1;ndez A, Burgos H, Mondaca M, Barra R, N&amp;#xFA;&amp;#xF1;ez H, P&amp;#xE9;rez H, Soto-Moyano R, Sierralta W, Fern&amp;#xE1;ndez V, Olivares R, Valladares L
    Reduction of the protein content from 25 to 8% casein in the diet of pregnant rats results in impaired neocortical long-term potentiation (LTP) of the offspring together with lower visuospatial memory performance. The present study was aimed to investigate whether this type of maternal malnutrition could result in modification of plastic capabilities of the entorhinal cortex (EC) in the adult progeny. Unlike normal eutrophic controls, 55-60-day-old prenatally malnourished rats were unable to develop LTP in the medial EC to tetanizing stimulation delivered to either the ipsilateral occipital cortex or the CA1 hippocampal region....</description>
            <author>Neural Plasticity</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1597337</comments>
            <pubDate>Wed, 09 Jul 2008 14:12:11 +0100</pubDate>
            <guid isPermaLink="false">1597337</guid>        </item>
        <item>
            <title>Differential Induction of Long-Term Potentiation in the Horizontal versus Columnar Superficial Connections to Layer II Cells of the Entorhinal Cortex.</title>
            <link>http://www.medworm.com/index.php?rid=1597336&amp;cid=s_36794_25_f&amp;fid=36794&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D18604300%26dopt%3DAbstract</link>
            <description>Authors: Ma L, Alonso A, Dickson CT
    The entorhinal cortex (EC) is a nodal and independent mnemonic element of the medial temporal lobe memory circuit as it forms a bidirectional interface between the neocortex and hippocampus. Within the EC, intra- and inter-lamellar associational connections occur via horizontal and columnar projections, respectively. We undertook a comparative study of these two inputs as they converge upon EC layer II cells using whole-cell patch techniques in an adult rat EC horizontal slice preparation in which the deepest layers (V-VI) had been dissected out. Electrical stimulation of layers I and III during GABA blockade allowed us to study excitatory synaptic properties and plasticity in the horizontal and columnar fibre systems, respectively. Both pathways exh...</description>
            <author>Neural Plasticity</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1597336</comments>
            <pubDate>Wed, 09 Jul 2008 14:12:11 +0100</pubDate>
            <guid isPermaLink="false">1597336</guid>        </item>
        <item>
            <title>Complementary Roles of Hippocampus and Medial Entorhinal Cortex in Episodic Memory</title>
            <link>http://www.medworm.com/index.php?rid=1582412&amp;cid=s_36794_168_f&amp;fid=37050&amp;url=http%3A%2F%2Fwww.hindawi.com%2FGetArticle.aspx%3Fdoi%3D10.1155%2F2008%2F258467</link>
            <description>Spatial mapping and navigation are figured prominently in the extant literature that describes hippocampal function. The medial entorhinal cortex is likewise attracting increasing interest, insofar as evidence accumulates that this area also contributes to spatial information processing. Here, we discuss recent electrophysiological findings that offer an alternate view of hippocampal and medial entorhinal function. These findings suggest complementary contributions of the hippocampus and medial entorhinal cortex in support of episodic memory, wherein hippocampal networks encode sequences of events that compose temporally and spatially extended episodes, whereas medial entorhinal networks disambiguate overlapping episodes by binding sequential events into distinct memories. (Source: Neural ...</description>
            <author>Neural Plasticity</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1582412</comments>
            <pubDate>Sun, 06 Jul 2008 11:57:42 +0100</pubDate>
            <guid isPermaLink="false">1582412</guid>        </item>
        <item>
            <title>Differential Induction of Long-Term Potentiation in the Horizontal versus Columnar Superficial Connections to Layer II Cells of the Entorhinal Cortex</title>
            <link>http://www.medworm.com/index.php?rid=1554963&amp;cid=s_36794_168_f&amp;fid=37050&amp;url=http%3A%2F%2Fwww.hindawi.com%2FGetArticle.aspx%3Fdoi%3D10.1155%2F2008%2F814815</link>
            <description>The entorhinal cortex (EC) is a nodal and independent mnemonic element of the medial temporal lobe memory circuit as it forms a bidirectional interface between the neocortex and hippocampus. Within the EC, intra- and inter-lamellar associational connections occur via horizontal and columnar projections, respectively. We undertook a comparative study of these two inputs as they converge upon EC layer II cells using whole-cell patch techniques in an adult rat EC horizontal slice preparation in which the deepest layers (V-VI) had been dissected out. Electrical stimulation of layers I and III during GABA blockade allowed us to study excitatory synaptic properties and plasticity in the horizontal and columnar fibre systems, respectively. Both pathways exhibited AMPA- and NMDA-receptor mediated ...</description>
            <author>Neural Plasticity</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1554963</comments>
            <pubDate>Mon, 30 Jun 2008 12:48:04 +0100</pubDate>
            <guid isPermaLink="false">1554963</guid>        </item>
        <item>
            <title>Effect of Prenatal Protein Malnutrition on Long-Term Potentiation and BDNF Protein Expression in the Rat Entorhinal Cortex after Neocortical and Hippocampal Tetanization</title>
            <link>http://www.medworm.com/index.php?rid=1554962&amp;cid=s_36794_168_f&amp;fid=37050&amp;url=http%3A%2F%2Fwww.hindawi.com%2FGetArticle.aspx%3Fdoi%3D10.1155%2F2008%2F646919</link>
            <description>Reduction of the protein content from 25 to 8&amp;#37; casein in the diet of pregnant rats results in impaired neocortical long-term potentiation (LTP) of the offspring together with lower visuospatial memory performance. The present study was aimed to investigate whether this type of maternal malnutrition could result in modification of plastic capabilities of the entorhinal cortex (EC) in the adult progeny. Unlike normal eutrophic controls, 55&amp;#8211;60-day-old prenatally malnourished rats were unable to develop LTP in the medial EC to tetanizing stimulation delivered to either the ipsilateral occipital cortex or the CA1 hippocampal region. Tetanizing stimulation of CA1 also failed to increase the concentration of brain-derived neurotrophic factor (BDNF) in the EC of 
malnourished rats. Impai...</description>
            <author>Neural Plasticity</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1554962</comments>
            <pubDate>Mon, 30 Jun 2008 12:48:04 +0100</pubDate>
            <guid isPermaLink="false">1554962</guid>        </item>
        <item>
            <title>The role of the entorhinal cortex in extinction: influences of aging.</title>
            <link>http://www.medworm.com/index.php?rid=1552512&amp;cid=s_36794_25_f&amp;fid=36794&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D18584042%26dopt%3DAbstract</link>
            <description>Authors: Bevilaqua LR, Rossato JI, Bonini JS, Myskiw JC, Clarke JR, Monteiro S, Lima RH, Medina JH, Cammarota M, Izquierdo I
    The entorhinal cortex is perhaps the area of the brain in which neurofibrillary tangles and amyloid plaques are first detectable in old age with or without mild cognitive impairment, and very particularly in Alzheimer's disease. It plays a key role in memory formation, retrieval, and extinction, as part of circuits that include the hippocampus, the amygdaloid nucleus, and several regions of the neocortex, in particular of the prefrontal cortex. Lesions or biochemical impairments of the entorhinal cortex hinder extinction. Microinfusion experiments have shown that glutamate NMDA receptors, calcium and calmodulin-dependent protein kinase II, and protein synthesis i...</description>
            <author>Neural Plasticity</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1552512</comments>
            <pubDate>Sat, 28 Jun 2008 18:03:14 +0100</pubDate>
            <guid isPermaLink="false">1552512</guid>        </item>
        <item>
            <title>The Role of the Entorhinal Cortex in Extinction: Influences of Aging</title>
            <link>http://www.medworm.com/index.php?rid=1536828&amp;cid=s_36794_168_f&amp;fid=37050&amp;url=http%3A%2F%2Fwww.hindawi.com%2FGetArticle.aspx%3Fdoi%3D10.1155%2F2008%2F595282</link>
            <description>The entorhinal cortex is perhaps the area of the brain in which neurofibrillary tangles and amyloid plaques are first detectable in old age with or without mild cognitive impairment, and very particularly in Alzheimer&amp;#39;s disease. It plays a key role in memory formation, retrieval, and extinction, as part of circuits that include the hippocampus, the amygdaloid nucleus, and several regions of the neocortex, in particular of the prefrontal cortex. Lesions or biochemical impairments of the entorhinal cortex hinder extinction. Microinfusion experiments have shown that glutamate NMDA receptors, calcium and calmodulin-dependent protein kinase II, and protein synthesis in the entorhinal cortex are involved in and required for extinction. Aging also hinders extinction; it is possible that its e...</description>
            <author>Neural Plasticity</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1536828</comments>
            <pubDate>Sun, 22 Jun 2008 22:04:28 +0100</pubDate>
            <guid isPermaLink="false">1536828</guid>        </item>
        <item>
            <title>Enhancement of neocortical-medial temporal EEG correlations during non-REM sleep.</title>
            <link>http://www.medworm.com/index.php?rid=1536092&amp;cid=s_36794_25_f&amp;fid=36794&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D18566693%26dopt%3DAbstract</link>
            <description>Authors: Axmacher N, Helmstaedter C, Elger CE, Fell J
    Interregional interactions of oscillatory activity are crucial for the integrated processing of multiple brain regions. However, while the EEG in virtually all brain structures passes through substantial modifications during sleep, it is still an open question whether interactions between neocortical and medial temporal EEG oscillations also depend on the state of alertness. Several previous studies in animals and humans suggest that hippocampal-neocortical interactions crucially depend on the state of alertness (i.e., waking state or sleep). Here, we analyzed scalp and intracranial EEG recordings during sleep and waking state in epilepsy patients undergoing presurgical evaluation. We found that the amplitudes of oscillations within...</description>
            <author>Neural Plasticity</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1536092</comments>
            <pubDate>Sat, 21 Jun 2008 23:01:51 +0100</pubDate>
            <guid isPermaLink="false">1536092</guid>        </item>
    </channel>
</rss>

