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        <title>Synapse 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 'Synapse' source.</description>
        <link><![CDATA[http://www.medworm.com/rss/search.php?qu=Synapse&t=Synapse&s=Search&f=source]]></link>
        <lastBuildDate>Wed, 08 Feb 2012 20:43:35 +0100</lastBuildDate>
        <item>
            <title>Role of perisynaptic parameters in neurotransmitter homeostasis ‐ computational study of a general synapse</title>
            <link>http://www.medworm.com/index.php?rid=5668751&amp;cid=s_33785_25_f&amp;fid=33785&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fsyn.21547</link>
            <description>AbstractExtracellular neurotransmitter concentrations vary over a wide range depending on the type of neurotransmitter and location in the brain. Neurotransmitter homeostasis near a synapse is achieved by a balance of several mechanisms including vesicular release from the presynapse, diffusion, uptake by transporters, non‐synaptic production, and regulation of release by autoreceptors. These mechanisms are also affected by the glia surrounding the synapse. However, the role of these mechanisms in achieving neurotransmitter homeostasis is not well understood. A biophysical modeling framework was proposed, based on a cortico‐accumbens synapse example case, to reverse engineer glial configurations and parameters related to homeostasis for synapses that support a range of neurotransmitter...</description>
            <author>Synapse</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5668751</comments>
            <pubDate>Thu, 09 Feb 2012 01:26:33 +0100</pubDate>
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        <item>
            <title>Transient increases in dendritic spine density contribute to dentate gyrus long‐term potentiation</title>
            <link>http://www.medworm.com/index.php?rid=5668753&amp;cid=s_33785_25_f&amp;fid=33785&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fsyn.21545</link>
            <description>AbstractDendritic spines are the primary sites for excitatory neurotransmission in the adult brain and exhibit changes in their number and morphology with experience. The relationship between spine formation and synaptic activity has been best characterized along the apical dendrites of pyramidal neurons in the hippocampal CA1 subfield. However, less is known about the structural mechanisms at the spine that mediate plasticity in other hippocampal subfields. The dentate gyrus is the predominant point of entry for synaptic input to the hippocampus, and dentate granule cells differ from CA1 pyramidal neurons in terms of their morphology and biophysical properties. In order to understand the structural mechanisms for plasticity in the dentate gyrus, we measured dendritic spine density in hipp...</description>
            <author>Synapse</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5668753</comments>
            <pubDate>Wed, 08 Feb 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5668753</guid>        </item>
        <item>
            <title>Effects of amphetamine on subcellular distribution of dopamine and DOPAC</title>
            <link>http://www.medworm.com/index.php?rid=5668752&amp;cid=s_33785_25_f&amp;fid=33785&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fsyn.21546</link>
            <description>AbstractAmphetamine effects on distribution of dopamine, DOPAC, and amphetamine in vesicular, cytosolic, and extracellular compartments associated with a striatal varicosity were estimated through use of a computer simulation model. In addition, contribution to overall effects of amphetamine by each of five actions – transport by dopamine transporter, transport by vesicular monoamine transporter, stimulation of reverse transport, inhibition of monoamine oxidase, and slowing of dopamine cell firing rate – were evaluated. Amphetamine enters a varicosity almost entirely by dopamine transporter and accumulates to very high levels within the varicosity. Both reverse transport by dopamine transporter and passive diffusion contribute to continual amphetamine egress across the plasma membrane....</description>
            <author>Synapse</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5668752</comments>
            <pubDate>Wed, 08 Feb 2012 05:00:00 +0100</pubDate>
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        <item>
            <title>Pharmacological characterization of the norepinephrine and dopamine reuptake inhibitor EB‐1020: Implications for treatment of attention‐deficit hyperactivity disorder</title>
            <link>http://www.medworm.com/index.php?rid=5650118&amp;cid=s_33785_25_f&amp;fid=33785&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fsyn.21538</link>
            <description>(Source: Synapse)</description>
            <author>Synapse</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5650118</comments>
            <pubDate>Fri, 03 Feb 2012 01:27:58 +0100</pubDate>
            <guid isPermaLink="false">5650118</guid>        </item>
        <item>
            <title>Changes in GABA and GABAB receptor expressions are involved in neuropathy in the rat cuneate nucleus following median nerve transection</title>
            <link>http://www.medworm.com/index.php?rid=5650124&amp;cid=s_33785_25_f&amp;fid=33785&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fsyn.21539</link>
            <description>This study examined the relationship between changes in GABA transmission and behavioral abnormalities after median nerve transection. Following unilateral median nerve transection, the percentage of GABA‐like immunoreactive neurons in the cuneate nucleus and that of GABAB receptor‐like immunoreactive neurons in the dorsal root ganglion in the injured side decreased and reached a nadir at 4 weeks after median nerve transection. Four weeks after bilateral median nerve transection and intraperitoneal application with saline, baclofen (2 mg/kg), or phaclofen (2 mg/kg) before unilateral electrical stimulation of the injured median nerve, we investigated the level of neuropeptide Y release and c‐Fos expression in the stimulated side of the cuneate nucleus. The neuropeptide Y release level...</description>
            <author>Synapse</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5650124</comments>
            <pubDate>Tue, 31 Jan 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5650124</guid>        </item>
        <item>
            <title>A new trick of INPP4A: Decreased expression of INPP4A in patients with temporal lobe epilepsy and pilocarpine‐induced rat model</title>
            <link>http://www.medworm.com/index.php?rid=5650123&amp;cid=s_33785_25_f&amp;fid=33785&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fsyn.21540</link>
            <description>AbstractInositol polyphosphate phosphatase 4 A (INPP4A), a phosphoinositides phosphatase, is highly expressed in the central nervous system and plays a role in glutamate excitotoxicity and cell proliferation. Our aim was to investigate the expression of INPP4A in patients with temporal lobe epilepsy (TLE) and in a rat model of epilepsy. We assessed the expression of INPP4A in the temporal neocortex from twenty TLE patients. The result showed that INPP4A expression was significantly lower in TLE patients than in controls. To validate the results found in TLE patients, we assessed the expression of INPP4A in rat model. Rat epilepsy was induced by lithium‐pilocarpine. Expression of INPP4A of rat models was assessed by immunohistochemistry, immunofluorescence and Western blotting. INPP4A was...</description>
            <author>Synapse</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5650123</comments>
            <pubDate>Tue, 31 Jan 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5650123</guid>        </item>
        <item>
            <title>Evaluation and initial in vitro and ex vivo characterisation of the potential positron emission tomography ligand, BU99008 (2‐(4,5‐Dihydro‐1H‐imidazol‐2‐yl)‐1‐methyl‐1H‐indole), for the Imidazoline2 binding site</title>
            <link>http://www.medworm.com/index.php?rid=5650122&amp;cid=s_33785_25_f&amp;fid=33785&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fsyn.21541</link>
            <description>AbstractThe density of the Imidazoline2 binding site (I2BS) has been shown to change in psychiatric conditions such as depression and addiction, along with neurodegenerative disorders such as Alzheimer's disease and Huntington's chorea. The presence of I2BS on glial cells and the possibility that they may in some way regulate glial fibrillary acidic protein (GFAP), has led to increased interest into the role of I2BS and I2BS ligands in conditions characterised by marked gliosis. In addition, it has been suggested that I2BS may be a marker for human glioblastomas. Therefore the development of a positron emission tomography (PET) radioligand for the I2BS would be of major benefit in our understanding of these conditions. We now report the successful synthesis and initial pharmacological eval...</description>
            <author>Synapse</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5650122</comments>
            <pubDate>Tue, 31 Jan 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5650122</guid>        </item>
        <item>
            <title>Test‐retest stability of cerebral mGluR5 quantification using [11C]ABP688 and PET in rats</title>
            <link>http://www.medworm.com/index.php?rid=5650121&amp;cid=s_33785_25_f&amp;fid=33785&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fsyn.21542</link>
            <description>In conclusion, our results suggest that non‐invasive quantification of [11C]ABP688 imaging is reproducible and reliable for PET studies of the cerebral mGluR5 in rats. Synapse, 2012. © 2012 Wiley‐Liss, Inc. (Source: Synapse)</description>
            <author>Synapse</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5650121</comments>
            <pubDate>Tue, 31 Jan 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5650121</guid>        </item>
        <item>
            <title>Longitudinal and parallel monitoring of neuroinflammation and neurodegeneration in a 6‐hydroxydopamine rat model of Parkinson's disease</title>
            <link>http://www.medworm.com/index.php?rid=5650120&amp;cid=s_33785_25_f&amp;fid=33785&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fsyn.21543</link>
            <description>AbstractAs neuroinflammatory processes are involved in the pathogenesis of Parkinson's disease (PD), we achieved the longitudinal evaluation of them in parallel with the modifications of dopaminergic function at several time‐points after 6‐hydroxydopamine (6‐OHDA) lesion in the rat mimicking an early stage of PD. After unilateral intra‐striatal 6‐OHDA administration, we quantified the temporal evolution of the 18 kDa translocator protein (TSPO), TH‐immunoreactivity and dopamine transporters in the striatum and substantia nigra pars compacta (SNc) from 3 to 56 days post‐lesion (dpl). Increased binding of TSPO ligands used, i.e. [3H]PK11195 and [125I]CLINDE, was observed in the lesioned striatum at 3, 7 and 14 dpl, followed by a progressive return to the basal level at 56 dpl. ...</description>
            <author>Synapse</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5650120</comments>
            <pubDate>Tue, 31 Jan 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5650120</guid>        </item>
        <item>
            <title>D1‐NMDA receptor interactions in the rat nucleus accumbens change during adolescence</title>
            <link>http://www.medworm.com/index.php?rid=5650119&amp;cid=s_33785_25_f&amp;fid=33785&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fsyn.21544</link>
            <description>AbstractMany aspects of the dopamine (DA) system mature during adolescence. For example, the DA modulation of glutamate responses in the rat prefrontal cortex (PFC) acquires adult characteristics during late adolescence. In the striatum, D1 receptors modulate NMDA responses, but whether this behaviorally important interaction matures during adolescence is not known. Here, we tested whether the D1 agonist SKF38393 affects NMDA actions on nucleus accumbens medium spiny neuron (MSN) excitability in slices from juvenile and young adult rats. NMDA dose‐dependently increased excitability in both age groups, and the D1 agonist produced a marginal increase of MSN excitability. In juvenile slices, the most common interaction was a downregulation of NMDA effects on excitability by the D1 agonist, ...</description>
            <author>Synapse</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5650119</comments>
            <pubDate>Tue, 31 Jan 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5650119</guid>        </item>
        <item>
            <title>Locomotor behavior of bonnet monkeys after spinal contusion injury: Footprint study</title>
            <link>http://www.medworm.com/index.php?rid=5599475&amp;cid=s_33785_25_f&amp;fid=33785&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fsyn.21537</link>
            <description>AbstractAnalysis of gait functions following spinal cord injury has been widely studied in rats, mice but limited in primates. The current investigation was performed to quantitatively analyze the degree of functional recovery in bipedal locomotion in bonnet monkeys after induced spinal cord contusion. The degree of locomotor recovery was examined by measuring four gait variables, viz., tip of opposite foot (TOF), print‐length (PL), toe‐spread (TS) and intermediary toe‐spread (IT) from the recorded hindlimb prints of monkeys using ink and paper technique. Contusion was induced in spinal cord at T12‐L1 level in anaesthetized monkeys by using the Allen's weight drop technique. Postoperatively, all spinal contused animals initially showed a significant decrease in TOF, which then grad...</description>
            <author>Synapse</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5599475</comments>
            <pubDate>Wed, 18 Jan 2012 02:14:20 +0100</pubDate>
            <guid isPermaLink="false">5599475</guid>        </item>
        <item>
            <title>Simultaneous measurement of extracellular dopamine and dopamine transporter occupancy by cocaine analogs in squirrel monkeys</title>
            <link>http://www.medworm.com/index.php?rid=5599476&amp;cid=s_33785_25_f&amp;fid=33785&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fsyn.21536</link>
            <description>AbstractSeveral classes of drugs bind to the dopamine transporter (DAT) with high affinity, but some are weaker positive reinforcers than cocaine, suggesting that affinity for and occupancy of the DAT is not the only determinant of a drug's reinforcing effectiveness. Other factors such as the rate of onset have been positively and strongly correlated with the reinforcing effects of DAT inhibitors in nonhuman primates. In the current studies, we examined the effects of acute systemic administration of cocaine and three cocaine analogs (RTI‐150, RTI‐177, and RTI‐366) on binding to DAT in squirrel monkey brain using PET neuroimaging. During the PET scan, we also measured drug effects on dopamine (DA) levels in the caudate using in vivo microdialysis. In general, our results suggest a la...</description>
            <author>Synapse</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5599476</comments>
            <pubDate>Thu, 12 Jan 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5599476</guid>        </item>
        <item>
            <title>Affinity and selectivity of [11C]‐(+)‐PHNO for the D3 and D2 receptors in the rhesus monkey brain in vivo</title>
            <link>http://www.medworm.com/index.php?rid=5545631&amp;cid=s_33785_25_f&amp;fid=33785&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fsyn.21535</link>
            <description>AbstractThough [11C]‐(+)‐PHNO has enabled quantification of the dopamine‐D3 receptor (D3R) in the human brain in vivo, its selectivity for the D3R is not sufficiently high to allow us to disregard its binding to the dopamine‐D2 receptor (D2R). We quantified the affinity of [11C]‐(+)‐PHNO for the D2R and D3R in the living primate brain. Two rhesus monkeys were examined on four occasions each, with [11C]‐(+)‐PHNO administered in a bolus + infusion paradigm Varying doses of unlabelled (+)‐PHNO were co‐administered on each occasion (total doses ranging from 0.09 to 5.61 μg/kg). The regional binding potential (BPND) and the corresponding doses of injected (+)‐PHNO were used as inputs in a model which quantified the affinity of (+)‐PHNO for the D2R and D3R, as well as th...</description>
            <author>Synapse</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5545631</comments>
            <pubDate>Wed, 28 Dec 2011 17:38:53 +0100</pubDate>
            <guid isPermaLink="false">5545631</guid>        </item>
        <item>
            <title>Correlation of the vesicular acetylcholine transporter densities in the striata to the clinical abilities of women with rett syndrome (RTT)</title>
            <link>http://www.medworm.com/index.php?rid=5545640&amp;cid=s_33785_25_f&amp;fid=33785&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fsyn.21515</link>
            <description>AbstractRett syndrome (RTT) is a neurodevelopmental disability characterized by mutations in the X‐linked methyl‐CpG‐binding protein 2 (MeCP2) located at the Xq28 region. The severity is modified in part by X chromosomal inactivation resulting in wide clinical variability. We hypothesized that the ability to perform the activities of daily living (ADL) is correlated with the density of vesicular acetylcholine transporters in the striata of women with RTT. The density of the vesicular acetylcholine transporters in the living human brain can be estimated by single‐photon emission‐computed tomography (SPECT) after the administration of (‐)‐5‐[123I]iodobenzovesamicol ([123I]IBVM).Twenty‐four (24) hours following the intravenous injection of approximately 333 MBq (9 mCi) [123I...</description>
            <author>Synapse</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5545640</comments>
            <pubDate>Wed, 28 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5545640</guid>        </item>
        <item>
            <title>In vivo dopaminergic and behavioural responses to acute cocaine are altered in adenosine A2A receptor knockout mice</title>
            <link>http://www.medworm.com/index.php?rid=5545639&amp;cid=s_33785_25_f&amp;fid=33785&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fsyn.21527</link>
            <description>AbstractAdenosine, acting on A2A adenosine receptors, regulates addictive processes induced by drugs of abuse. The present study investigates the role of A2A adenosine receptors in neurochemical and behavioural responses to an acute cocaine challenge.Changes in the extracellular levels of dopamine in the nucleus accumbens of mice lacking A2A adenosine receptors and wild type littermates after an acute cocaine (20mg/kg) administration were evaluated by in vivo microdialysis studies. Locomotor effects induced by cocaine were measured during the microdialysis procedure.Cocaine‐evoked increases in extracellular dopamine were not sustained in mice lacking A2A receptors in comparison to wild‐type mice (P&amp;lt;0.05). Cocaine administration significantly increased ambulatory activity in both gen...</description>
            <author>Synapse</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5545639</comments>
            <pubDate>Wed, 28 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5545639</guid>        </item>
        <item>
            <title>Adolescent female rats exhibiting activity‐based anorexia express elevated levels of GABAA receptor α4 and δ subunits at the plasma membrane of hippocampal CA1 spines</title>
            <link>http://www.medworm.com/index.php?rid=5545638&amp;cid=s_33785_25_f&amp;fid=33785&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fsyn.21528</link>
            <description>AbstractActivity‐based anorexia (ABA) is an animal model for anorexia nervosa that has revealed genetic links to anxiety traits and neurochemical characteristics within the hypothalamus. However, few studies have used this animal model to investigate the biological basis for vulnerability of pubertal and adolescent females to ABA, even though the great majority of the anorexia nervosa cases are females exhibiting the first symptoms during puberty. GABAergic inhibition of the hippocampus strongly regulates anxiety as well as plasticity throughout life. We recently showed that the hippocampal CA1 of female mice undergo a dramatic change at puberty onset – from expressing virtually none of the non‐synaptic α4βδ GABAA receptors (GABARs) pre‐pubertally to expressing these GABARs at a...</description>
            <author>Synapse</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5545638</comments>
            <pubDate>Wed, 28 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5545638</guid>        </item>
        <item>
            <title>Effect of transient blockade of N‐methyl‐D‐aspartate receptors at neonatal stage on stress‐induced lactate metabolism in the medial prefrontal cortex of adult rats: Role of 5‐HT1A receptor agonism</title>
            <link>http://www.medworm.com/index.php?rid=5545637&amp;cid=s_33785_25_f&amp;fid=33785&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fsyn.21529</link>
            <description>AbstractDecreased activity of the prefrontal cortex (mPFC) has been considered a basis for core symptoms of schizophrenia, an illness associated with a neurodevelopmental origin. Evidence from preclinical and clinical studies indicates serotonin (5‐HT)1A receptors play a crucial role in the energy metabolism of the mPFC. The present study was undertaken to determine 1) if transient blockade of N‐methyl‐D‐aspartate (NMDA) receptors during the neonatal stage inhibit energy demands in response to stress, as measured by extracellular lactate concentrations, in the mPFC at the young adult stage, and 2) if tandospirone, a 5‐HT1A partial agonist, reverses the effect of the neonatal insult on energy metabolism. Male pups received MK‐801 (0.20 mg/kg) on postnatal day (PD) 7 through 10. ...</description>
            <author>Synapse</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5545637</comments>
            <pubDate>Wed, 28 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5545637</guid>        </item>
        <item>
            <title>Nicotinic acetylcholine receptors in rat forebrain that bind 18F‐nifene: Relating PET imaging, autoradiography and behavior</title>
            <link>http://www.medworm.com/index.php?rid=5545636&amp;cid=s_33785_25_f&amp;fid=33785&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fsyn.21530</link>
            <description>In this study we used the novel compound 18F‐nifene to examine the distribution of nAChRs in the rat forebrain, and for individual animals related the results to behavioral performance on an auditory‐cognitive task. We first show negligible binding of 18F‐nifene in mice lacking the β2 nAChR subunit, consistent with previous findings that 18F‐nifene binds to α4β2* nAChRs. We then examined the distribution of 18F‐nifene in rat using three methods: in vivo PET, ex vivo PET and autoradiography. Generally, 18F‐nifene labeled forebrain regions known to contain nAChRs, and the three methods produced similar relative binding among regions. Importantly, 18F‐nifene also labeled some white matter (myelinated axon) tracts, most prominently in the temporal subcortical region that conta...</description>
            <author>Synapse</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5545636</comments>
            <pubDate>Wed, 28 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5545636</guid>        </item>
        <item>
            <title>Effects of the triple reuptake inhibitor amitifadine on extracellular levels of monoamines in rat brain regions and on locomotor activity</title>
            <link>http://www.medworm.com/index.php?rid=5545635&amp;cid=s_33785_25_f&amp;fid=33785&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fsyn.21531</link>
            <description>AbstractMajor depressive disorder is a prevalent disease and current pharmacotherapy is considered to be inadequate. It has been hypothesized that a triple reuptake inhibitor (TRI) that activates dopamine neurotransmission in addition to serotonin and norepinephrine circuitries may result in enhanced antidepressant effects. Here we investigated the pharmacological effects of a serotonin‐preferring TRI ‐ amitifadine (EB‐1010, formerly DOV 21947). The effects of amitifadine (10 mg/kg ip.) on extracellular concentrations of monoamines and their metabolites in rat brain regions were investigated using the in vivo microdialysis technique. The effects of amitifadine on locomotor activity and stereotyped behavior were also evaluated. A major metabolite of amitifadine, the 2‐lactam compoun...</description>
            <author>Synapse</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5545635</comments>
            <pubDate>Wed, 28 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5545635</guid>        </item>
        <item>
            <title>Effects of mirtazapine on sleep disturbance under neuropathic pain‐like state</title>
            <link>http://www.medworm.com/index.php?rid=5545634&amp;cid=s_33785_25_f&amp;fid=33785&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fsyn.21532</link>
            <description>AbstractSleep disturbance has been reported to be one of the most frequent symptoms in patients suffered from severe pain. Benzodiazepines are effective and reduce anxiety in the hours after use, but the induced sleep tends to be less than ideal in quality, with increased stage I‐II and reduces stage III‐IV sleep. In the present study, we investigated sleep disturbance under a neuropathic pain‐like state in mice using electroencephalogram (EEG) / electromyogram (EMG). In a model of neuropathic pain, sciatic nerve ligation caused a marked decrease in the latency of paw withdrawal in response to a thermal stimulus only on the ipsilateral side. Under this condition, sciatic nerve‐ligated animals showed a statistically significant increase in wakefulness and a decrease in non‐rapid e...</description>
            <author>Synapse</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5545634</comments>
            <pubDate>Wed, 28 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5545634</guid>        </item>
        <item>
            <title>Aging‐related deficits in orexin/hypocretin modulation of the septo‐hippocampal cholinergic system</title>
            <link>http://www.medworm.com/index.php?rid=5545633&amp;cid=s_33785_25_f&amp;fid=33785&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fsyn.21533</link>
            <description>AbstractThe medial septum (MS) of the basal forebrain contains cholinergic neurons that project to the hippocampus, support cognitive function, and are implicated in age‐related cognitive decline. Hypothalamic orexin/hypocretin neurons innervate and modulate basal forebrain cholinergic neurons and provide direct inputs to the hippocampus. However, the precise role of orexin in modulating hippocampal cholinergic transmission—and how these interactions are altered in aging—is unknown. Here, orexin A was administered to CA1 and the MS of young (3‐4 months) and aged (27‐29 months) Fisher 344/Brown Norway rats, and hippocampal acetylcholine efflux was analyzed by in vivo microdialysis. At both infusion sites orexin A dose‐dependently increased hippocampal acetylcholine in young, but...</description>
            <author>Synapse</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5545633</comments>
            <pubDate>Wed, 28 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5545633</guid>        </item>
        <item>
            <title>Synaptic vesicle recycling is enhanced by torsinA that harbors the DYT1 dystonia mutation</title>
            <link>http://www.medworm.com/index.php?rid=5545632&amp;cid=s_33785_25_f&amp;fid=33785&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fsyn.21534</link>
            <description>AbstractEarly‐onset generalized dystonia, DYT1, is caused by a mutation in the gene encoding the evolutionarily conserved AAA+ ATPase torsinA. Synaptic abnormalities have been implicated in DYT1 dystonia, but the details of the synaptic pathophysiology are only partially understood. Here, we demonstrate a novel role for torsinA in synaptic vesicle recycling, using cultured hippocampal neurons from a knock‐in mouse model of DYT1 dystonia (ΔE‐torsinA) and live‐cell imaging with styryl FM dyes. Neurons from heterozygous ΔE‐torsinA mice released a larger fraction of the total recycling pool (TRP) during a single round of electrical stimulation than did wild‐type neurons. Moreover, when the neurons were subjected to prior high activity, the time course of release was shortened. In...</description>
            <author>Synapse</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5545632</comments>
            <pubDate>Wed, 28 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5545632</guid>        </item>
        <item>
            <title>Positron emission tomography (PET) experience with 2‐[18F]Fluoro‐3‐(2(S)‐azetidinylmethoxy)pyridine (2‐[18F]FA) in the living human brain of smokers with paranoid schizophrenia</title>
            <link>http://www.medworm.com/index.php?rid=5506819&amp;cid=s_33785_25_f&amp;fid=33785&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fsyn.21520</link>
            <description>AbstractUtilizing postmortem data (Breese, et al., 2000), we hypothesized that the densities of high‐affinity neuronal α4β2 nicotinic acetylcholine receptors (nAChRs) in the brain exist in a continuum from highest to lowest as follows: smokers without schizophrenia &amp;gt; smokers with schizophrenia &amp;gt; nonsmokers without schizophrenia &amp;gt; nonsmokers with schizophrenia. Application of the Kruskal‐Wallis Test (Stata, 2003) to the postmortem data (Breese, et al., 2000) confirmed the hypothesized order in the cortex and the hippocampus and attained significance in the caudate and the thalamus.Positron emission tomography (PET) was performed for 60 minutes at 6 hours after the intravenous administration of 444 megabequerels [MBq] (12 mCi) 2‐[18F]fluoro‐3‐(2(S)‐azetidinylmethoxy)py...</description>
            <author>Synapse</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5506819</comments>
            <pubDate>Fri, 16 Dec 2011 13:51:45 +0100</pubDate>
            <guid isPermaLink="false">5506819</guid>        </item>
        <item>
            <title>Restoring cerebral dopamine homeostasis by electrical forepaw stimulation: An FMRI study</title>
            <link>http://www.medworm.com/index.php?rid=5553329&amp;cid=s_33785_25_f&amp;fid=33785&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fsyn.21516</link>
            <description>This study shows not only the capacity of peripheral stimulation to perturb neurotransmitter function, but also the potential of peripheral stimulation to restore neurotransmitter homeostasis. Synapse, 2011. © 2011 Wiley Periodicals, Inc. (Source: Synapse)</description>
            <author>Synapse</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5553329</comments>
            <pubDate>Tue, 13 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5553329</guid>        </item>
        <item>
            <title>Positron emission tomography experience with 2‐[18F]fluoro‐3‐(2(s)‐azetidinylmethoxy)pyridine (2‐[18F]fa) in the living human brain of smokers with paranoid schizophrenia</title>
            <link>http://www.medworm.com/index.php?rid=5553328&amp;cid=s_33785_25_f&amp;fid=33785&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fsyn.21520</link>
            <description>AbstractUtilizing postmortem data (Breese et al. [2000] Neuropsychopharmacology 23:351–364), we hypothesized that the densities of high‐affinity neuronal α4β2 nicotinic acetylcholine receptors (nAChRs) in the brain exist in a continuum from highest to lowest as follows: smokers without schizophrenia &amp;gt; smokers with schizophrenia &amp;gt; nonsmokers without schizophrenia &amp;gt; nonsmokers with schizophrenia. Application of the Kruskal‐Wallis Test (Statacorp, 2003) to the postmortem data (Breese et al. [2000] Neuropsychopharmacology 23:351‐364) confirmed the hypothesized order in the cortex and the hippocampus and attained significance in the caudate and the thalamus. Positron emission tomography (PET) was performed for 60 min at 6 h after the intravenous administration of 444 megabequ...</description>
            <author>Synapse</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5553328</comments>
            <pubDate>Tue, 13 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5553328</guid>        </item>
        <item>
            <title>Restoring cerebral dopamine homeostasis by electrical forepaw stimulation: an fMRI study effect of forepaw stimulation in PD brain</title>
            <link>http://www.medworm.com/index.php?rid=5506823&amp;cid=s_33785_25_f&amp;fid=33785&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fsyn.21516</link>
            <description>This study shows not only the capacity of peripheral stimulation to perturb neurotransmitter function, but also the potential of peripheral stimulation to restore neurotransmitter homeostasis. Synapse, 2011. © 2011 Wiley‐Liss, Inc. (Source: Synapse)</description>
            <author>Synapse</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5506823</comments>
            <pubDate>Tue, 13 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5506823</guid>        </item>
        <item>
            <title>Dendritic morphology of neurons in prefrontal cortex and ventral hippocampus of rats with neonatal amygdala lesion</title>
            <link>http://www.medworm.com/index.php?rid=5506822&amp;cid=s_33785_25_f&amp;fid=33785&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fsyn.21517</link>
            <description>AbstractNeonatal basolateral amygdala (nBLA) lesions in rats have been widely used as a neurodevelopmental model that mimics schizophrenia‐like behaviors. Recently, we reported that nBLA lesions result in significant decreases in the dendritic spine number of layer 3 PFC pyramidal cells and medium spiny neurons of the NAcc, which all changes after puberty. At present, we aimed to evaluate the effect of this lesion in pyramidal neurons of CA1 of the ventral hippocampus (VH) and layer 5 of the PFC. In order to assess the effects of nBLA lesions on the dendritic morphology of the PFC and VH neurons, we carried out nBLA lesions in rats on postnatal day (PD) 7, and then we studied the dendritic morphology of these two limbic subregions at prepubertal (PD35) and postpubertal (PD60) ages. Dendr...</description>
            <author>Synapse</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5506822</comments>
            <pubDate>Tue, 13 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5506822</guid>        </item>
        <item>
            <title>Electroconvulsive seizures stimulate the VEGF pathway via mTORC1</title>
            <link>http://www.medworm.com/index.php?rid=5506821&amp;cid=s_33785_25_f&amp;fid=33785&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fsyn.21518</link>
            <description>AbstractElectroconvulsive treatment (ECT) is considered the most effective treatment of depression. Recent studies demonstrate that electroconvulsive seizures (ECS), the animal variant of ECT, robustly stimulate hippocampal cell proliferation. However, the mechanisms underlying the cellular and molecular responses to ECS are not yet fully understood. A leading hypothesis of depression suggests that neurotrophic factors/growth factors play a critical role. Particularly the vascular endothelial growth factor (VEGF) is considered important, as it has been demonstrated that hippocampal VEGF expression is induced by ECS and that signaling through the VEGF receptor, Flk‐1 (VEGFR2), is required for cell proliferation. VEGF expression is believed to be regulated by two distinct mTOR (mammalian T...</description>
            <author>Synapse</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5506821</comments>
            <pubDate>Tue, 13 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5506821</guid>        </item>
        <item>
            <title>Sucrose‐predictive cues evoke greater phasic dopamine release than saccharin‐predictive cues</title>
            <link>http://www.medworm.com/index.php?rid=5506820&amp;cid=s_33785_25_f&amp;fid=33785&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fsyn.21519</link>
            <description>AbstractCues that have been paired with food evoke dopamine in nucleus accumbens (NAc) and drive approach behavior. This cue‐evoked dopamine signaling could contribute to overconsumption of food. One manner in which individuals try to restrict caloric intake is through the consumption of foods containing artificial (non‐nutritive) sweeteners. We were interested in whether cues paired with a non‐nutritive sweetener (saccharin) would evoke similar dopamine release as cues paired with a nutritive sweetener (sucrose). We trained food‐restricted rats to associate distinct cues with sucrose or saccharin pellets. In the first group of rats, training sessions with each pellet took place on different days, maximizing the opportunity for rats to detect nutritional differences. After training...</description>
            <author>Synapse</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5506820</comments>
            <pubDate>Tue, 13 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5506820</guid>        </item>
        <item>
            <title>Sciatic nerve repair by acellular nerve xenografts implanted with BMSCs in rats</title>
            <link>http://www.medworm.com/index.php?rid=5459587&amp;cid=s_33785_25_f&amp;fid=33785&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fsyn.21508</link>
            <description>In conclusion, ANX implanted with BMSCs could replace allografts to promote nerve regeneration effectively, which offers a reliable approach for repairing peripheral nerve defects. Synapse, 2011. © 2011 Wiley‐Liss, Inc. (Source: Synapse)</description>
            <author>Synapse</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5459587</comments>
            <pubDate>Thu, 01 Dec 2011 14:22:08 +0100</pubDate>
            <guid isPermaLink="false">5459587</guid>        </item>
        <item>
            <title>Sciatic nerve repair by acellular nerve xenografts implanted with BMSCs in rats xenograft combined with BMSCs</title>
            <link>http://www.medworm.com/index.php?rid=5506825&amp;cid=s_33785_25_f&amp;fid=33785&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fsyn.21508</link>
            <description>In conclusion, ANX implanted with BMSCs could replace allografts to promote nerve regeneration effectively, which offers a reliable approach for repairing peripheral nerve defects. Synapse, 2011. © 2011 Wiley Periodicals, Inc. (Source: Synapse)</description>
            <author>Synapse</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5506825</comments>
            <pubDate>Wed, 30 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5506825</guid>        </item>
        <item>
            <title>In vivo evaluation in cynomolgus monkey brain and metabolism of [18F]fluorodeprenyl: A new MAO‐B pet radioligand</title>
            <link>http://www.medworm.com/index.php?rid=5553327&amp;cid=s_33785_25_f&amp;fid=33785&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fsyn.21514</link>
            <description>In this study, we evaluated the in vivo characteristics of a new monoamine oxidase type B (MAO‐B) radioligand, [18F]fluorodeprenyl, by positron emission tomography (PET) in two cynomolgus monkeys. The brain uptake of [18F]fluorodeprenyl was more than 7% (600% SUV) of the total injected radioactivity and similar to that of [11C]deprenyl, an established MAO‐B radioligand. The highest uptake was observed in the striatum, one of the MAO‐B‐rich regions, with a peak at approximately 2–3 min after injection, followed by lower uptake in the thalamus and the cortex and lowest uptake in the cerebellum. Brain uptake of [18F]fluorodeprenyl was largely inhibited by preadministration of the MAO‐B inhibitor, L‐deprenyl, whereas clorgyline, a MAO Type A blocker, had no significant inhibitory...</description>
            <author>Synapse</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5553327</comments>
            <pubDate>Tue, 29 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5553327</guid>        </item>
        <item>
            <title>In vivo evaluation in cynomolgus monkey brain and metabolism of [18F]fluorodeprenyl a new MAO‐B PET radioligand</title>
            <link>http://www.medworm.com/index.php?rid=5459588&amp;cid=s_33785_25_f&amp;fid=33785&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fsyn.21514</link>
            <description>In this study we evaluated the in vivo characteristics of a new MAO‐B radioligand, [18F]fluorodeprenyl, by positron emission tomography (PET) in two cynomolgus monkeys. The brain uptake of [18F]fluorodeprenyl was over 7% (600% SUV) of the total injected radioactivity and similar to that of [11C]deprenyl, an established MAO‐B radioligand. The highest uptake was observed in the striatum, one of the MAO‐B rich regions, with a peak at approximately 2‐3 min after injection, followed by lower uptake in the thalamus, the cortex and lowest uptake in the cerebellum. Brain uptake of [18F]fluorodeprenyl was largely inhibited by pre‐administration of the MAO‐B inhibitor, L‐deprenyl, whereas clorgyline, a MAO‐A blocker, had no significant inhibitory effect, thus demonstrating selectivit...</description>
            <author>Synapse</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5459588</comments>
            <pubDate>Tue, 29 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5459588</guid>        </item>
        <item>
            <title>Ultrastructural synaptic changes associated with neurofibromatosis type 1: A quantitative analysis of hippocampal region CA1 in a Nf1+/− Mouse Model</title>
            <link>http://www.medworm.com/index.php?rid=5450332&amp;cid=s_33785_25_f&amp;fid=33785&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fsyn.21507</link>
            <description>AbstractNeurofibromatosis type 1 (NF1) is one of the most frequently diagnosed autosomal dominant inherited disorders resulting in neurological dysfunction, including an assortment of learning disabilities and cognitive deficits. To elucidate the neural mechanisms underlying the disorder, we employed a mouse model (Nf1+/−) to conduct a quantitative analysis of ultrastructural changes associated with the NF1 disorder. Using both serial light and electron microscopy, we examined reconstructions of the CA1 region of the hippocampus, which is known to play a central role in many of the dysfunctions associated with NF1. In general, the morphology of synapses in both the Nf1+/− and wild‐type groups of animals were similar. No differences were observed in synapse per neuron density, pre‐ ...</description>
            <author>Synapse</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5450332</comments>
            <pubDate>Mon, 28 Nov 2011 13:57:24 +0100</pubDate>
            <guid isPermaLink="false">5450332</guid>        </item>
        <item>
            <title>Immunocytochemical localization of calretinin‐containing neurons in the rat periaqueductal gray and colocalization with enzymes producing nitric oxide: A double, double‐labeling study</title>
            <link>http://www.medworm.com/index.php?rid=5553330&amp;cid=s_33785_25_f&amp;fid=33785&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fsyn.21509</link>
            <description>AbstractThe pattern of distribution and colocalization of the calcium‐binding protein calretinin (Cal) and of enzymes producing nitric oxide (NO) was examined in the rat periaqueductal gray matter (PAG) using two different experimental approaches, by combining Cal immunocytochemistry with NADPH‐diaphorase (NADPH‐d) histochemistry and with NOS immunocytochemistry, respectively. Cal‐immunopositive neurons were found throughout the rostrocaudal extension of both dorsolateral (PAG‐dl) and ventrolateral PAG (PAG‐vl). Double‐labeled neurons were found only in PAG‐dl. The first experimental approach indicated that 33–41% of the NADPH‐d‐positive (Nadph+) cells were immunoreactive for Cal, whereas NADPH‐d activity appeared in 19–26% of the Cal‐immunopositive (CalIP) neur...</description>
            <author>Synapse</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5553330</comments>
            <pubDate>Mon, 28 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5553330</guid>        </item>
        <item>
            <title>Augmentation by escitalopram, but not citalopram or R‐citalopram, of the effects of low‐dose risperidone: Behavioral, biochemical, and electrophysiological evidence</title>
            <link>http://www.medworm.com/index.php?rid=5506824&amp;cid=s_33785_25_f&amp;fid=33785&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fsyn.21510</link>
            <description>We examined antipsychotic efficacy using the conditioned avoidance response (CAR) test, extrapyramidal side effect (EPS) liability using a catalepsy test, dopamine outflow in the medial prefrontal cortex (mPFC) and nucleus accumbens using in vivo microdialysis in freely moving animals, and NMDA receptor‐mediated transmission in the mPFC using intracellular electrophysiological recording in vitro. Only escitalopram (5 mg/kg), but not citalopram (10 mg/kg), or R‐citalopram (10 mg/kg), dramatically enhanced the antipsychotic‐like effect of a low dose of risperidone (0.25 mg/kg), without increasing catalepsy. Given alone, escitalopram, but not citalopram or R‐citalopram, markedly enhanced both cortical dopamine output and NMDA receptor‐mediated transmission. Addition of escitalopram ...</description>
            <author>Synapse</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5506824</comments>
            <pubDate>Mon, 28 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5506824</guid>        </item>
        <item>
            <title>Immunocytochemical localization of calretinin‐containing neurons in the rat periaqueductal gray and co‐localization with enzymes producing nitric oxide (NO): a double, double‐labeling study</title>
            <link>http://www.medworm.com/index.php?rid=5450337&amp;cid=s_33785_25_f&amp;fid=33785&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fsyn.21509</link>
            <description>AbstractThe pattern of distribution and co‐localization of the calcium binding protein calretinin (Cal) and of enzymes producing nitric oxide (NO) was examined in the rat periaqueductal gray matter (PAG) using two different experimental approaches, by combining Cal immunocytochemistry with NADPH‐diaphorase (NADPH‐d) histochemistry and with NOS immunocytochemistry, respectively. Cal‐immunopositive neurons were found throughout the rostrocaudal extension of both dorsolateral (PAG‐dl) and ventrolateral PAG (PAL‐vl). Double‐labeled neurons were found only in PAG‐dl. The first experimental approach indicated that 33%‐41% of the NADPH‐d‐positive (Nadph+) cells were immunoreactive for Cal whereas NADPH‐d activity appeared in 19%‐26% of the Cal‐immunopositive (CalIP) ne...</description>
            <author>Synapse</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5450337</comments>
            <pubDate>Mon, 28 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5450337</guid>        </item>
        <item>
            <title>Augmentation by escitalopram, but not citalopram or R‐citalopram, of the effects of low dose risperidone. Behavioral, biochemical and electrophysiological evidence</title>
            <link>http://www.medworm.com/index.php?rid=5450336&amp;cid=s_33785_25_f&amp;fid=33785&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fsyn.21510</link>
            <description>We examined antipsychotic efficacy using the conditioned avoidance response (CAR) test, extrapyramidal side effect (EPS) liability using a catalepsy test, dopamine outflow in the medial prefrontal cortex (mPFC) and nucleus accumbens using in vivo microdialysis in freely moving animals, and NMDA receptor‐mediated transmission in the mPFC using intracellular electrophysiological recording in vitro. Only escitalopram (5 mg/kg), but not citalopram (10 mg/kg) or R‐citalopram (10 mg/kg), dramatically enhanced the antipsychotic‐like effect of a low dose of risperidone (0.25 mg/kg), without increasing catalepsy. Given alone, escitalopram, but not citalopram or R‐citalopram, markedly enhanced both cortical dopamine output and NMDA receptor‐mediated transmission. Addition of escitalopram a...</description>
            <author>Synapse</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5450336</comments>
            <pubDate>Mon, 28 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5450336</guid>        </item>
        <item>
            <title>The comparative effects of environmental enrichment with exercise and serotonin transporter blockade on serotonergic neurons in the dorsal raphe nucleus</title>
            <link>http://www.medworm.com/index.php?rid=5450335&amp;cid=s_33785_25_f&amp;fid=33785&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fsyn.21511</link>
            <description>AbstractWe have previously reported that inhibition of the serotonin transporter (SERT) by selective serotonin reuptake inhibitor (SSRI) fluoxetine significantly reduces the number of tryptophan hydroxylase (TPH)‐positive cells in the dorsal raphe nucleus. We have been interested in exploring whether this SSRI‐induced change in TPH might be modified by housing in an enriched environment. Like SSRI antidepressants, environmental enrichment (EE) and physical exercise have been found to have efficacy in the prevention and alleviation of depression. We postulated that EE with exercise and SERT inhibition would similarly affect TPH regulation and that EE with exercise might modify the effect of fluoxetine on TPH. Three week old male Sprague‐Dawley rats were housed in either a standard cag...</description>
            <author>Synapse</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5450335</comments>
            <pubDate>Mon, 28 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5450335</guid>        </item>
        <item>
            <title>Prenatal stress alters dendritic morphology and synaptic connectivity in the prefrontal cortex and hippocampus of developing offspring</title>
            <link>http://www.medworm.com/index.php?rid=5450334&amp;cid=s_33785_25_f&amp;fid=33785&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fsyn.21512</link>
            <description>AbstractThe current study used stereological techniques in combination with Golg‐Cox methods to examine the neuroanatomical alterations in the prefrontal cortex and hippocampus of developing offspring exposed to gestational stress. Morphological changes in dendritic branching, length, and spine density, were examined at weaning along with changes in actual numbers of neurons. Using this information we generated a gross estimation of synaptic connectivity. The results showed region‐specific and sex‐dependent alterations to neuroanatomy in response to prenatal stress. The two regions of the prefrontal cortex, medial prefrontal and orbital prefrontal cortices, exhibited sexually dimorphic, opposite changes, in synaptic connectivity in response to the same experience. Both male and femal...</description>
            <author>Synapse</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5450334</comments>
            <pubDate>Mon, 28 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5450334</guid>        </item>
        <item>
            <title>Methamphetamine self‐administration acutely decreases monoaminergic transporter function</title>
            <link>http://www.medworm.com/index.php?rid=5450333&amp;cid=s_33785_25_f&amp;fid=33785&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fsyn.21506</link>
            <description>In conclusion, the present manuscript is the first to describe transporter function and METH/AMPH levels after self‐administration in rodents. These data provide a foundation to investigate complex questions including how the response of dopaminergic systems to METH self‐administration contributes to contingent‐related processes such as dependence. Synapse, 2011. © 2011 Wiley‐Liss, Inc. (Source: Synapse)</description>
            <author>Synapse</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5450333</comments>
            <pubDate>Mon, 28 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5450333</guid>        </item>
        <item>
            <title>[3H]Chiba‐1001(Methyl‐SSR180711) has low in vitro binding affinity and poor in vivo selectivity to nicotinic alpha‐7 receptor in rodent brain</title>
            <link>http://www.medworm.com/index.php?rid=5443024&amp;cid=s_33785_25_f&amp;fid=33785&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fsyn.21513</link>
            <description>AbstractNeuronal nicotinic acetylcholine receptor (nAChR) agonists active at the alpha‐7 (α‐7) receptor subtype are potential therapeutics for cognitive deficits in schizophrenia, Alzheimer's disease and other mental disorders. SSR180711, an α‐7 selective partial agonist, has been shown to improve preclinical cognition. A novel PET radioligand, 11C‐Chiba1001, is a close analogue of SSR180711, We labeled Chiba‐1001 with tritium in order to evaluate its utility as a preclinical radioligand tool . In vitro, the binding affinity of [3H]Chiba‐1001 at the α‐7 receptor was low (Kd = 120 to 180 nM) in both HEK239 cell membranes expressing human α‐7 receptor and in native rat hippocampus membranes. The α‐7 selective ligands AZD0328, ARR17779 and MLA did not inhibit [3H]Chiba...</description>
            <author>Synapse</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5443024</comments>
            <pubDate>Fri, 25 Nov 2011 13:47:27 +0100</pubDate>
            <guid isPermaLink="false">5443024</guid>        </item>
        <item>
            <title>Involvement of the cGMP pathway in the osthole‐facilitated glutamate release in rat hippocampal nerve endings</title>
            <link>http://www.medworm.com/index.php?rid=5365473&amp;cid=s_33785_25_f&amp;fid=33785&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fsyn.21505</link>
            <description>AbstractOsthole, an active constituent isolated from Cnidium monnieri (L.) Cusson, has previously been shown to have the capacity to increase depolarization‐evoked glutamate release in rat hippocampal nerve terminals. As cGMP‐dependent signaling cascade has been found to modulate glutamate release at the presynaptic level, the aim of this study was to further examine the role of cGMP signaling pathway in the regulation of osthole on glutamate release in hippocampal synaptosomes. Results showed that osthole dose‐dependently increased intrasynaptosomal cGMP levels. The elevation of cGMP levels by osthole was prevented by the phosphodiesterase 5 inhibitor sildenafil, but was insensitive to the guanylyl cyclase inhibitor ODQ. In addition, osthole‐induced facilitation of 4‐aminopyridi...</description>
            <author>Synapse</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5365473</comments>
            <pubDate>Thu, 03 Nov 2011 23:27:41 +0100</pubDate>
            <guid isPermaLink="false">5365473</guid>        </item>
        <item>
            <title>Regulation of type 1 inositol 1,4,5‐triphosphate receptor by dopamine receptors in cocaine‐induced place conditioning</title>
            <link>http://www.medworm.com/index.php?rid=5423765&amp;cid=s_33785_25_f&amp;fid=33785&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fsyn.20997</link>
            <description>This study investigated the role and regulation of IP3R‐1 in mice with cocaine‐induced place preference. The cocaine‐induced place preference was dose‐dependently inhibited by intracerebroventricular pretreatment with IP3R antagonists, 2‐aminophenoxyethane‐borate (2‐APB), and xestospongin C. The levels of IP3R‐1 in the frontal cortex and nucleus accumbens of cocaine‐conditioned mice significantly increased, which was completely abolished by SCH23390 and sulpiride, selective dopamine D1 and D2 receptor antagonists, respectively. These findings suggest that IP3R‐1‐mediated intracellular signaling pathway may play an important role in the development of cocaine‐induced place preference and that the expression of IP3R‐1 is controlled by both dopamine D1 and D2 recepto...</description>
            <author>Synapse</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5423765</comments>
            <pubDate>Thu, 27 Oct 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5423765</guid>        </item>
        <item>
            <title>Olanzapine suppresses the rewarding and discriminative stimulus effects induced by morphine</title>
            <link>http://www.medworm.com/index.php?rid=5365479&amp;cid=s_33785_25_f&amp;fid=33785&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fsyn.21500</link>
            <description>AbstractAtypical antipsychotic medications are effective for treating both the positive and negative symptoms of schizophrenia. Olanzapine is an atypical antipsychotic that blocks dopaminergic, serotonergic, adrenergic, histaminergic, and muscarinic receptors. In the present study, we used rodents to investigate whether olanzapine could suppress the hyperlocomotion, rewarding effect and discriminative stimulus effect induced by the prototypic μ‐opioid morphine, which are all considered to reflect the abuse potential or psychoactive effects of μ‐opioids. Olanzapine at doses that failed to induce motor coordination produced a dose‐dependent reduction in hyperlocomotion induced by morphine in mice. Olanzapine at a dose that did not produce motor dysfunction also inhibited the signific...</description>
            <author>Synapse</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5365479</comments>
            <pubDate>Thu, 27 Oct 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5365479</guid>        </item>
        <item>
            <title>Increased affinity of dopamine for D2‐like versus D1‐like receptors. Relevance for volume transmission in interpreting PET findings</title>
            <link>http://www.medworm.com/index.php?rid=5365478&amp;cid=s_33785_25_f&amp;fid=33785&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fsyn.21501</link>
            <description>AbstractEvidence indicates that dopamine (DA) mainly acts as a Volume Transmission (VT) transmitter through its release into the extracellular fluid where the D1‐like and D2‐like receptors are predominantly extrasynaptic. It was therefore of interest to compare the affinities of the 2 major families of DA receptors. [3H] raclopride /DA and [3H] SCH23390/DA competition assays compared the affinity of DA at D2‐like and D1‐like receptors in rat dorsal striatal membrane preparations as well as in membrane preparations from CHO cell lines stably transfected with human D2L and D1 receptors. The IC50 values of DA at D2‐like receptors in dorsal striatal membranes and CHO cell membranes were markedly and significantly reduced compared to the IC50 values of DA at D1‐like receptors. These...</description>
            <author>Synapse</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5365478</comments>
            <pubDate>Thu, 27 Oct 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5365478</guid>        </item>
        <item>
            <title>Immunohistochemical localization of enkephalin in the human striatum: A postmortem ultrastructural study</title>
            <link>http://www.medworm.com/index.php?rid=5365477&amp;cid=s_33785_25_f&amp;fid=33785&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fsyn.21502</link>
            <description>AbstractWithin the basal ganglia, the functionally defined region referred to as the striatum contains a subset of GABAergic medium spiny neurons expressing the neuropeptide enkephalin. Although the major features of ultrastructural enkephalin localization in striatum have been characterized among various species, its ultrastructural organization has never been studied in the human brain. Human striatal tissue was obtained from the Maryland and Alabama Brain Collections from 8 normal controls. The brains were received and fixed within 8 hours of death allowing for excellent preservation suitable for electron microscopy. Tissue from the dorsal striatum was processed for enkephalin immunoreactivity, and prepared for electron microscopy. General morphology of the dorsal striatum was consisten...</description>
            <author>Synapse</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5365477</comments>
            <pubDate>Thu, 27 Oct 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5365477</guid>        </item>
        <item>
            <title>Cell membrane lytic action of metoclopramide and its relation to tardive dyskinesia</title>
            <link>http://www.medworm.com/index.php?rid=5365476&amp;cid=s_33785_25_f&amp;fid=33785&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fsyn.21504</link>
            <description>AbstractThe long‐term use of many antipsychotic medications carries a risk of tardive dyskinesia in a small proportion of patients. Although metoclopramide is an antipsychotic at high doses, this drug is more commonly used at low daily doses to accelerate stomach movement of food. Because prolonged use of metoclopramide has also been associated with tardive dyskinesia, this drug is convenient to study in order to examine the possible basis of tardive dyskinesia. Previous work proposed that antipsychotics accumulated in the melanin granules of the human substantia nigra, ultimately building up to high concentrations that could disrupt cell membranes of nigral neurons. While previous work demonstrated the accumulation of metoclopramide in post‐mortem human nigral tissue, it remained to b...</description>
            <author>Synapse</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5365476</comments>
            <pubDate>Thu, 27 Oct 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5365476</guid>        </item>
        <item>
            <title>Type 1 inositol 1,4,5‐trisphosphate receptor expression is regulated by dopamine receptors in mouse brain with cocaine‐induced place conditioning</title>
            <link>http://www.medworm.com/index.php?rid=5365475&amp;cid=s_33785_25_f&amp;fid=33785&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fsyn.20997</link>
            <description>AbstractRecent study shows that type 1 inositol‐1, 4, 5‐triphosohate receptors (IP3Rs) may be involved in amphetamine‐induced conditioned preference, but little is known about its role in psychological dependence on cocaine. The present study investigated the role and regulation of IP3R‐1 in mice with cocaine‐induced place preference. The cocaine‐induced place preference was dose‐dependently inhibited by intracerebroventricular pretreatment with IP3R antagonists, 2‐aminophenoxyethane‐borate (2‐APB) and xestospongin C. The levels of IP3R‐1 in the frontal cortex and nucleus accumbens of cocaine‐conditioned mice significantly increased, which was completely abolished by SCH23390 and sulpiride, selective dopamine D1 and D2 receptor antagonists, respectively. These findi...</description>
            <author>Synapse</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5365475</comments>
            <pubDate>Thu, 27 Oct 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5365475</guid>        </item>
        <item>
            <title>Dopaminergic modulation of nitric oxide synthase activity in subregions of the rat nucleus accumbens</title>
            <link>http://www.medworm.com/index.php?rid=5365474&amp;cid=s_33785_25_f&amp;fid=33785&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fsyn.21503</link>
            <description>In this study, the impact of pharmacological manipulations of D1, D2 and NMDA receptors on nNOS activity was determined using optical density measures of NADPH‐d staining preformed in multiple subdivisions (core, medial shell, intermediate shell and lateral shell) of the NAc. Awake behaving rats received systemic administration of vehicle and/or the following drugs ∼25 minutes prior to tissue harvesting: the nNOS inhibitor NG‐propyl‐L‐arginine (NPA), the D1 receptor agonist SKF 81297, the D1 receptor antagonist SCH 23390, the D2 receptor agonist quinpirole (QNP), the D2 receptor antagonist eticlopride (ETI), or the NMDA receptor antagonist CPP. In vehicle treated animals a distinct medial‐lateral histochemical gradient of NADPH‐d staining was observed which was characterized ...</description>
            <author>Synapse</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5365474</comments>
            <pubDate>Thu, 27 Oct 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5365474</guid>        </item>
        <item>
            <title>Gestational IV nicotine produces elevated brain‐derived neurotrophic factor in the mesocorticolimbic dopamine system of adolescent rat offspring</title>
            <link>http://www.medworm.com/index.php?rid=5306019&amp;cid=s_33785_25_f&amp;fid=33785&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fsyn.20975</link>
            <description>AbstractMaternal smoking during pregnancy is associated with enduring psychopathology, such as increased likelihood of substance use, in offspring. Various animal models demonstrate that continuous nicotine exposure produces teratogenic effects in offspring, as well. In this experiment, a novel intravenous (IV) exposure model was used to determine if gestational nicotine (GN) treatment produced alterations in methamphetamine‐induced sensitization and the expression of brain‐derived neurotrophic factor (BDNF) in the mesocorticolimbic dopamine (DA) system of adolescent offspring. Dams were injected with IV saline or nicotine (0.05 mg/kg/injection) three times per day on gestational days 8–21. Habituation was measured on postnatal day (PND) 25–27 and baseline activity on PND 28. On PN...</description>
            <author>Synapse</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5306019</comments>
            <pubDate>Wed, 12 Oct 2011 13:31:50 +0100</pubDate>
            <guid isPermaLink="false">5306019</guid>        </item>
        <item>
            <title>Imaging of dopamine D2/3 agonist binding in cocaine dependence: A [11C]NPA positron emission tomography study</title>
            <link>http://www.medworm.com/index.php?rid=5306018&amp;cid=s_33785_25_f&amp;fid=33785&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fsyn.20970</link>
            <description>Conclusions: The results of this [11C]NPA PET study do not support alterations in D2/3 HIGH binding in the striatum in cocaine dependence. Synapse, 2011. © 2011 Wiley‐Liss, Inc. (Source: Synapse)</description>
            <author>Synapse</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5306018</comments>
            <pubDate>Wed, 12 Oct 2011 13:31:39 +0100</pubDate>
            <guid isPermaLink="false">5306018</guid>        </item>
        <item>
            <title>Combination strategies for repair, plasticity, and regeneration using regulation of gene expression during the chronic phase after spinal cord injury</title>
            <link>http://www.medworm.com/index.php?rid=5306017&amp;cid=s_33785_25_f&amp;fid=33785&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fsyn.20903</link>
            <description>This study seeks to elucidate the genetic underpinnings of SCI repair through the investigation of neurodegenerative and regenerative associated genes involved in the response to SCI during the chronic phase in adult rats. Intervention on the level of gene regulation focused on enhancing naturally attempting SCI regenerative genes has the potential to promote SCI repair. Our aim was to analyze gene expression characteristics of candidate genes involved in the neuro‐degenerative and ‐regenerative processes following various animal models of SCI. We compiled data showing gene expression changes after SCI in adult rats and created a chronological time‐line of candidate genes differentially expressed during the chronic phase of SCI. Compiled data showed that SCI induced a transient upreg...</description>
            <author>Synapse</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5306017</comments>
            <pubDate>Wed, 12 Oct 2011 13:31:25 +0100</pubDate>
            <guid isPermaLink="false">5306017</guid>        </item>
        <item>
            <title>DOPAC distribution and regulation in striatal dopaminergic varicosities and extracellular space</title>
            <link>http://www.medworm.com/index.php?rid=5306011&amp;cid=s_33785_25_f&amp;fid=33785&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fsyn.20996</link>
            <description>AbstractDOPAC, the major intermediate metabolite of dopamine, is found in the cytosolic compartment of dopaminergic terminals/varicosities and in the extracellular space. It has been proposed that extracellular DOPAC is derived from newly synthesized dopamine rather than from dopamine in the signaling pool. Based on literature data supporting such a concept, we hypothesize a DOPAC synthesis/secretory complex producing extracellular DOPAC and use a computational simulation model of dopaminergic varicosities to estimate the distribution of DOPAC between cytosolic and extracellular compartments, amount of newly synthesized dopamine entering the DOPAC synthesis/secretory complex, and potential regulatory processes in the complex. Results suggest that about two‐thirds of DOPAC is in the extra...</description>
            <author>Synapse</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5306011</comments>
            <pubDate>Wed, 12 Oct 2011 13:30:37 +0100</pubDate>
            <guid isPermaLink="false">5306011</guid>        </item>
        <item>
            <title>Hippocampal LTP triggers proteasome‐mediated SPAR degradation in CA1 neurons</title>
            <link>http://www.medworm.com/index.php?rid=5306013&amp;cid=s_33785_25_f&amp;fid=33785&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fsyn.20994</link>
            <description>AbstractActivity‐dependent synaptic plasticity is associated with synaptic protein turnover involving the ubiquitin proteasome system (UPS) for protein degradation. In primary hippocampal cell culture it has been shown that increased or decreased activity of synaptic transmission can regulate the amount of postsynaptic density (PSD) proteins via UPS. However, the specific spatio‐temporal dynamic of PSD protein degradation after LTP induction and its downstream signaling pathways remains to be clarify. We used confocal microscopy to monitor levels of eGFP‐tagged SPAR (spine‐associated Rap GTPase activating protein) expressed in acute hippocampal slices and found that LTP induction triggered a UPS‐dependent decay of eGFP‐SPAR fluorescence. SPAR degradation was reduced upon inhibi...</description>
            <author>Synapse</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5306013</comments>
            <pubDate>Mon, 10 Oct 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5306013</guid>        </item>
        <item>
            <title>Increased expression of histone deacetylases 2 in temporal lobe epilepsy: A study of epileptic patients and rat models</title>
            <link>http://www.medworm.com/index.php?rid=5306012&amp;cid=s_33785_25_f&amp;fid=33785&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fsyn.20995</link>
            <description>AbstractHistone deacetylases 2 (HDAC2) is expressed in the central nervous system; it has multiple functions in neural plasticity. However, we do not know if HDAC2 is also involved in the pathology of epilepsy. Here we report that HDAC2 was expressed in the brain tissues of both control and temporal lobe epilepsy (TLE) patients. Results from immunofluorescence and immunohistochemistry showed that HDAC2 was primarily located in the nucleus and that TLE patients exhibit significantly more HDAC2 positive cells than control. Western Blotting showed that HDAC2 protein levels were significantly higher in TLE than in control brain. Moreover, in the rat model of TLE, there was a sustained enhancement of HDAC2 expression in rat models of TLE. HDAC2 was significantly increased in both the acute (1d)...</description>
            <author>Synapse</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5306012</comments>
            <pubDate>Mon, 10 Oct 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5306012</guid>        </item>
        <item>
            <title>Granulocyte colony stimulating factor (G‐CSF) neuroprotective effects on spinal motoneurons after ventral root avulsion</title>
            <link>http://www.medworm.com/index.php?rid=5262683&amp;cid=s_33785_25_f&amp;fid=33785&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fsyn.20993</link>
            <description>In conclusion, the present results suggest that G‐CSF has an influence on the stability of pre‐synaptic terminals in the spinal cord as well as on the astroglial reaction, indicating a possible neuroprotective action. Synapse, 2011. © 2011 Wiley‐Liss, Inc. (Source: Synapse)</description>
            <author>Synapse</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5262683</comments>
            <pubDate>Thu, 29 Sep 2011 14:15:38 +0100</pubDate>
            <guid isPermaLink="false">5262683</guid>        </item>
        <item>
            <title>Granulocyte colony stimulating factor neuroprotective effects on spinal motoneurons after ventral root avulsion</title>
            <link>http://www.medworm.com/index.php?rid=5365480&amp;cid=s_33785_25_f&amp;fid=33785&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fsyn.20993</link>
            <description>In conclusion, the present results suggest that G‐CSF has an influence on the stability of presynaptic terminals in the spinal cord as well as on the astroglial reaction, indicating a possible neuroprotective action. Synapse, 2011. © 2011 Wiley‐Liss, Inc. (Source: Synapse)</description>
            <author>Synapse</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5365480</comments>
            <pubDate>Tue, 27 Sep 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5365480</guid>        </item>
        <item>
            <title>Study on molecular mechanism for improving neural regeneration after repair of sciatic nerve defect in rat by acellular nerve allograft</title>
            <link>http://www.medworm.com/index.php?rid=5262691&amp;cid=s_33785_25_f&amp;fid=33785&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fsyn.20985</link>
            <description>ConclusionsANA possessed fine histocompatibility, and might substitute autograft to repair long‐segment defect of sciatic nerve in rats. This action might be related to up‐regulation of protein and mRNA expression for BDNF and CGRP in spinal cord. Synapse, 2011. © 2011 Wiley‐Liss, Inc. (Source: Synapse)</description>
            <author>Synapse</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5262691</comments>
            <pubDate>Tue, 27 Sep 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5262691</guid>        </item>
        <item>
            <title>Chronic restraint stress affects serotonin transporter uptake kinetics but not binding sites in the rat hippocampus</title>
            <link>http://www.medworm.com/index.php?rid=5262690&amp;cid=s_33785_25_f&amp;fid=33785&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fsyn.20986</link>
            <description>(Source: Synapse)</description>
            <author>Synapse</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5262690</comments>
            <pubDate>Tue, 27 Sep 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5262690</guid>        </item>
        <item>
            <title>Dopamine agonist radioligand binds to both D2High and D2Low receptors, explaining why alterations in D2High are not detected in human brain scans</title>
            <link>http://www.medworm.com/index.php?rid=5262689&amp;cid=s_33785_25_f&amp;fid=33785&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fsyn.20987</link>
            <description>AbstractThe features of schizophrenia are consistent with increased sensitivity to endogenous dopamine. Animal models of schizophrenia reveal an increase in the in vitro proportion of striatal dopamine D2 receptors in the high‐affinity state for dopamine (i.e., D2High), as measured by dopamine/[3H]domperidone competition. However, in vivo studies did not reveal the dopamine agonist [11C](+)PHNO to be elevated in amphetamine‐sensitized rats. Also, no increase was found in the in vivo binding of [11C](+)PHNO in schizophrenia patients. The present work was done to resolve the contradictory findings. It was found that the in vitro density of rat striatal D2 receptors was 18 pmol/g for [3H]raclopride and 12 pmol/g for [3H](+)PHNO; most of the latter sites disappeared in the presence of guan...</description>
            <author>Synapse</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5262689</comments>
            <pubDate>Tue, 27 Sep 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5262689</guid>        </item>
        <item>
            <title>Cocaine induces the expression of MEF2C transcription factor in rat striatum through activation of SIK1 and phosphorylation of the histone deacetylase HDAC5</title>
            <link>http://www.medworm.com/index.php?rid=5262688&amp;cid=s_33785_25_f&amp;fid=33785&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fsyn.20988</link>
            <description>We report here that acute cocaine treatment of rats induced the expression of MEF2C in the striatum through a recently discovered transduction pathway. Repeated injections were found to induce MEF2C to a lesser extent. The mechanism by which MEF2C was induced involves the subsequent activation of the salt‐inducible kinase SIK1 and the phosphorylation of HDAC5, a member of the class IIa of HDACs. Cocaine activated SIK1 by phosphorylation on Thr‐182 residue, which was accompanied by the nuclear import of the kinase. In the nuclear compartment, SIK1 then phosphorylated HDAC5 causing the shuttling of its phospho‐form from the nucleus to the cytoplasm of striatal cells. Activation of SIK1 by cocaine was further validated by the phosphorylation of TORC1/3, which was followed by the shuttli...</description>
            <author>Synapse</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5262688</comments>
            <pubDate>Tue, 27 Sep 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5262688</guid>        </item>
        <item>
            <title>Running wheel exercise ameliorates methamphetamine‐induced damage to dopamine and serotonin terminals</title>
            <link>http://www.medworm.com/index.php?rid=5262687&amp;cid=s_33785_25_f&amp;fid=33785&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fsyn.20989</link>
            <description>AbstractRepeated administration of methamphetamine (mAMPH) to rodents in a single‐day “binge” produces long‐lasting damage to dopaminergic and serotonergic terminals. Because previous research has demonstrated that physical activity can ameliorate nigrostriatal injury, the present study investigated whether voluntary exercise in rats can alter the monoaminergic damage resulting from a neurotoxic mAMPH binge.Adult male rats were allowed constant access to running wheels or kept in non‐wheel cages for 3 weeks, then given a binge dosing regimen of mAMPH or saline. The rats were returned to their original environments for 3 additional weeks post‐mAMPH. [125I]RTI‐55 binding and autoradiography was used to quantify dopamine transporters (DAT), and radioimmunocytochemistry was used ...</description>
            <author>Synapse</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5262687</comments>
            <pubDate>Tue, 27 Sep 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5262687</guid>        </item>
        <item>
            <title>Slow phasic and tonic activity of ventral pallidal neurons during cocaine self‐administration</title>
            <link>http://www.medworm.com/index.php?rid=5262686&amp;cid=s_33785_25_f&amp;fid=33785&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fsyn.20990</link>
            <description>AbstractVentral pallidal (VP) neurons exhibit rapid phasic firing patterns within seconds of cocaine‐reinforced responses. The present investigation examined whether VP neurons exhibited firing rate changes: 1) over minutes during the inter‐infusion interval (slow phasic patterns) and/or 2) over the course of the several‐hour self‐administration session (tonic firing patterns) relative to pre‐session firing. Approximately two‐thirds (43/54) of VP neurons exhibited slow phasic firing patterns. The most common pattern was a post‐infusion decrease in firing followed by a progressive reversal of firing over minutes (51.16%; 22/43). Early reversals were predominantly observed anteriorly while progressive and late reversals were observed more posteriorly. Approximately half (51.85%...</description>
            <author>Synapse</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5262686</comments>
            <pubDate>Tue, 27 Sep 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5262686</guid>        </item>
        <item>
            <title>Subdiaphragmatic vagotomy induces a functional change in visceral Aδ primary afferent fibers in rats</title>
            <link>http://www.medworm.com/index.php?rid=5262685&amp;cid=s_33785_25_f&amp;fid=33785&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fsyn.20991</link>
            <description>(Source: Synapse)</description>
            <author>Synapse</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5262685</comments>
            <pubDate>Tue, 27 Sep 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5262685</guid>        </item>
        <item>
            <title>TRPV1 antagonist, A‐889425, inhibits mechanotransmission in a subclass of rat primary afferent neurons following peripheral inflammation</title>
            <link>http://www.medworm.com/index.php?rid=5262684&amp;cid=s_33785_25_f&amp;fid=33785&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fsyn.20992</link>
            <description>The objective of the current study was to characterize TRPV1‐mediated modulation of mechanically evoked activity in sensory axons innervating rat hind paws. We used an in vitro skin‐nerve preparation to record neural activity from single axons isolated from rat tibial nerve. Single fibers were classified by conduction velocity, mechanical threshold, and stimulus‐response relationships. We used A‐889425 to investigate uninjured and inflamed skin afferent neuron populations to evoked mechanical stimulation. Application of A‐889425 had no effect on the mechanical responsiveness of Aδ and C‐fiber units innervating uninjured skin. In contrast, A‐889425 inhibited responses of slowly conducting Aδ fiber units to noxious mechanical stimulation in a population of axons innervating C...</description>
            <author>Synapse</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5262684</comments>
            <pubDate>Tue, 27 Sep 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5262684</guid>        </item>
        <item>
            <title>Pre‐ and postsynaptic effects of norepinephrine on γ‐aminobutyric acid (GABA)‐ mediated synaptic transmission in layer 2/3 of the rat auditory cortex</title>
            <link>http://www.medworm.com/index.php?rid=5211255&amp;cid=s_33785_25_f&amp;fid=33785&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fsyn.20979</link>
            <description>In this study we used a combination of patch‐clamp recording and immunohistochemical techniques to identify the synaptic site and the location of the adrenergic receptors involved in the modulation of GABAergic signaling in cortical layer 2/3 of the rat.Our results showed that NE increases the frequency of spike‐independent miniature inhibitory postsynaptic currents (mIPSCs), as well as the probability of release of unitary inhibitory postsynaptic currents (IPSCs) obtained with patch‐clamp pair‐recordings. The pharmacology of mIPSCs and the identification of adrenergic receptors in neurons containing the GABAergic marker parvalbumin (PV) suggest that NE increases the presynaptic probability of GABA release by activating α2‐ and β‐receptors on PV‐positive neurons. On the con...</description>
            <author>Synapse</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5211255</comments>
            <pubDate>Tue, 13 Sep 2011 03:37:29 +0100</pubDate>
            <guid isPermaLink="false">5211255</guid>        </item>
        <item>
            <title>The acute administration of the selective dopamine D3 receptor antagonist SB‐277011A reverses conditioned place aversion produced by naloxone precipitated withdrawal from acute morphine administration in rats</title>
            <link>http://www.medworm.com/index.php?rid=5365481&amp;cid=s_33785_25_f&amp;fid=33785&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fsyn.20983</link>
            <description>We examined the effect of SB‐277011A, a selective D3 receptor antagonist, on the conditioned place aversion (CPA) response associated with naloxone‐induced withdrawal from acute morphine administration in male Sprague‐Dawley rats. Morphine (5.6 mg/kg i.p.) was given, followed 4 hrs later by naloxone (0.3 mg/kg i.p.) and prior to placing the animals in one specific chamber of the test apparatus. All animals were subjected to 2 of these trials. A significant CPA occurred in animals that received an i.p. injection of vehicle 30 minutes prior to the measurement of chamber preference. The pretreatment of animals (30 minutes prior to testing) with 3 mg/kg i.p. of SB‐277011A did not significantly alter the CPA compared to animals treated with vehicle (1 ml/kg i.p. of deionized distilled w...</description>
            <author>Synapse</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5365481</comments>
            <pubDate>Fri, 09 Sep 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5365481</guid>        </item>
        <item>
            <title>Striatal mitochondria in subjects with chronic undifferentiated vs. chronic paranoid schizophrenia</title>
            <link>http://www.medworm.com/index.php?rid=5306016&amp;cid=s_33785_25_f&amp;fid=33785&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fsyn.20981</link>
            <description>AbstractSchizophrenia (SZ) is a heterogeneous disease with a spectrum of symptoms, risk factors, and etiology. Abnormalities in mitochondria, the energy‐producing organelles of the cell, have been observed in mixed cohorts of subjects with SZ. The purpose of the present study was to determine if striatal mitochondria were differentially affected in two different DSM‐IV subgroups of SZ. Postmortem striatal tissue was examined from normal controls (NC), chronic paranoid SZs (SZP), and chronic undifferentiated SZs (SZU). Tissue was processed for calbindin immunohistochemistry to identify striosomal compartments, prepared for electron microscopy and analyzed using stereological methods. In both caudate and putamen, the density of mitochondria in the neuropil was decreased in SZP compared t...</description>
            <author>Synapse</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5306016</comments>
            <pubDate>Fri, 09 Sep 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5306016</guid>        </item>
        <item>
            <title>Pre‐ and postsynaptic effects of norepinephrine on γ‐aminobutyric acid‐mediated synaptic transmission in layer 2/3 of the rat auditory cortex</title>
            <link>http://www.medworm.com/index.php?rid=5306015&amp;cid=s_33785_25_f&amp;fid=33785&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fsyn.20979</link>
            <description>In this study, we used a combination of patch‐clamp recording and immunohistochemical techniques to identify the synaptic site and the location of the adrenergic receptors involved in the modulation of GABAergic signaling in cortical layer 2/3 of the rat. Our results showed that NE increases the frequency of spike‐independent miniature inhibitory postsynaptic currents (mIPSCs), as well as the probability of release of unitary inhibitory postsynaptic currents (IPSCs) obtained with patch‐clamp pair‐recordings. The pharmacology of mIPSCs and the identification of adrenergic receptors in neurons containing the GABAergic marker parvalbumin (PV) suggest that NE increases the presynaptic probability of GABA release by activating α2‐ and β‐receptors on PV‐positive neurons. On the c...</description>
            <author>Synapse</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5306015</comments>
            <pubDate>Fri, 09 Sep 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5306015</guid>        </item>
        <item>
            <title>Insights into the Sigma‐1 receptor chaperone's cellular functions: a microarray report</title>
            <link>http://www.medworm.com/index.php?rid=5211261&amp;cid=s_33785_25_f&amp;fid=33785&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fsyn.20984</link>
            <description>AbstractWe previously demonstrated that Sig‐1Rs are critical regulators in neuronal morphogenesis and development via the regulation of oxidative stress and mitochondrial functions. In the present study, we sought to identify pathways and genes that are affected by Sig‐1R. Gene expression profiles were examined in rat hippocampal neurons that had been cultured for18 days in vitro (DIV). The cells were transduced with AAV siRNA targeting Sig‐1R on DIV 10 for 7 days, followed by gene expression analysis using a rat genome cDNA array. The gene array results indicated that Sig‐1R knockdown hampered cellular functions including steroid biogenesis, protein ubiquitination, actin cytoskeleton network, and Nrf‐2 mediated oxidative stress. Many of the cellular components important for acti...</description>
            <author>Synapse</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5211261</comments>
            <pubDate>Fri, 09 Sep 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5211261</guid>        </item>
        <item>
            <title>The acute administration of the selective dopamine D3receptor antagonist SB‐ 277011‐A reverses conditioned place aversion produced by naloxone precipitated withdrawal from acute morphine administration in rats</title>
            <link>http://www.medworm.com/index.php?rid=5211260&amp;cid=s_33785_25_f&amp;fid=33785&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fsyn.20983</link>
            <description>(Source: Synapse)</description>
            <author>Synapse</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5211260</comments>
            <pubDate>Fri, 09 Sep 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5211260</guid>        </item>
        <item>
            <title>Subdiaphragmatic vagotomy increases the sensitivity of lumbar Aδ primary afferent neurons along with voltage‐dependent potassium channels in rats</title>
            <link>http://www.medworm.com/index.php?rid=5211259&amp;cid=s_33785_25_f&amp;fid=33785&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fsyn.20982</link>
            <description>AbstractSubdiaphragmatic vagal dysfunction causes chronic pain. To verify whether this chronic pain is accompanied by enhanced peripheral nociceptive sensitivity, we evaluated primary afferent neuronal excitability in subdiaphragmatic vagotomized (SDV) rats. SDV rats showed a decrease in the electrical stimuli‐induced hind limb‐flexion threshold at 250 Hz, but showed no similar effect at 5 Hz or 2000 Hz, which indicated that lumbar primary afferent Aδ sensitivity was enhanced in SDV rats. The whole‐cell patch‐clamp technique also revealed the hyper‐excitability of acutely dissociated medium‐sized lumbar dorsal root ganglion (DRG) neurons isolated from SDV rats. The contribution of changes in voltage‐dependent potassium (Kv) channels was assessed, and transient A‐type K+ (I...</description>
            <author>Synapse</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5211259</comments>
            <pubDate>Fri, 09 Sep 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5211259</guid>        </item>
        <item>
            <title>Striatal mitochondria in subjects with chronic undifferentiated versus chronic paranoid schizophrenia</title>
            <link>http://www.medworm.com/index.php?rid=5211257&amp;cid=s_33785_25_f&amp;fid=33785&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fsyn.20981</link>
            <description>AbstractSchizophrenia (SZ) is a heterogeneous disease with a spectrum of symptoms, risk factors and etiology. Abnormalities in mitochondria, the energy producing organelles of the cell, have been observed in mixed cohorts of subjects with SZ. The purpose of the present study was to determine if striatal mitochondria were differentially affected in two different DSM‐IV subgroups of SZ. Postmortem striatal tissue was examined from normal controls (NC), chronic paranoid SZs (SZP), and chronic undifferentiated SZs (SZU). Tissue was processed for calbindin immunohistochemistry to identify striosomal compartments, prepared for electron microscopy and analyzed using stereological methods. In both caudate and putamen, the density of mitochondria in the neuropil was decreased in SZP compared to b...</description>
            <author>Synapse</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5211257</comments>
            <pubDate>Fri, 09 Sep 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5211257</guid>        </item>
        <item>
            <title>Cortical spreading depression in alpha‐synuclein knockout mice</title>
            <link>http://www.medworm.com/index.php?rid=5211256&amp;cid=s_33785_25_f&amp;fid=33785&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fsyn.20980</link>
            <description>(Source: Synapse)</description>
            <author>Synapse</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5211256</comments>
            <pubDate>Fri, 09 Sep 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5211256</guid>        </item>
        <item>
            <title>Growth hormone increases neural cell adhesion polysialylation state in the dentate gyrus of γ‐irradiated rats</title>
            <link>http://www.medworm.com/index.php?rid=5185626&amp;cid=s_33785_25_f&amp;fid=33785&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fsyn.20945</link>
            <description>(Source: Synapse)</description>
            <author>Synapse</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5185626</comments>
            <pubDate>Sat, 03 Sep 2011 17:47:14 +0100</pubDate>
            <guid isPermaLink="false">5185626</guid>        </item>
        <item>
            <title>Gestational IV nicotine produces elevated BDNF in the mesocorticolimbic dopamine system of adolescent rat offspring</title>
            <link>http://www.medworm.com/index.php?rid=5176539&amp;cid=s_33785_25_f&amp;fid=33785&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fsyn.20975</link>
            <description>AbstractMaternal smoking during pregnancy is associated with enduring psychopathology, such as increased likelihood of substance use, in offspring. Various animal models demonstrate that continuous nicotine exposure produces teratogenic effects in offspring, as well. In the present experiment, a novel intravenous (IV) exposure model was utilized to determine if gestational nicotine (GN) treatment produced alterations in methamphetamine‐induced sensitization and the expression of brain derived neurotrophic factor (BDNF) in the mesocorticolimbic dopamine system of adolescent offspring. Dams were injected with IV saline or nicotine (0.05 mg/kg/injection) 3x/day on gestational days 8‐21. Habituation was measured on postnatal day (PND) 25‐27 and baseline activity on PND 28. On PND 29‐35...</description>
            <author>Synapse</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5176539</comments>
            <pubDate>Tue, 30 Aug 2011 17:56:56 +0100</pubDate>
            <guid isPermaLink="false">5176539</guid>        </item>
        <item>
            <title>Effects of perinatal asphyxia on rat striatal cytoskeleton</title>
            <link>http://www.medworm.com/index.php?rid=5147830&amp;cid=s_33785_25_f&amp;fid=33785&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fsyn.20978</link>
            <description>AbstractPerinatal asphyxia (PA) is a medical condition associated with a high short‐term morbimortality and different long term neurological diseases. In previous works, we have shown that neuronal and synaptic changes in rat striatum lead to ubi‐protein accumulation in post‐synaptic density (PSD) after six months of sub‐severe PA. However, very little is known about the synaptic and related structural modifications induced by PA in young rats. In the present work, we studied neuronal cytoskeleton modifications in striatum induced by sub‐severe PA in 30 days‐old rats. We observed a significant decrease in the number of neurons, in particular calbindin immunoreactive neurons after PA. In addition, it was also observed that actin cytoskeleton was highly modified in the PSD as wel...</description>
            <author>Synapse</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5147830</comments>
            <pubDate>Wed, 24 Aug 2011 14:12:48 +0100</pubDate>
            <guid isPermaLink="false">5147830</guid>        </item>
        <item>
            <title>Acetylcholine α7 nicotinic and dopamine D2 receptors are targeted to many of the same postsynaptic dendrites and astrocytes in the rodent prefrontal cortex</title>
            <link>http://www.medworm.com/index.php?rid=5147831&amp;cid=s_33785_25_f&amp;fid=33785&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fsyn.20977</link>
            <description>We examined the dual electron microscopic immunolabeling of α7nAChR and either D2R or the vesicular acetylcholine transporter (VAChT) in rodent PFC to assess convergent functional activation sites. Immunoreactivity (ir) for α7nAChR and/or D2R was seen in the same as well as separate neuronal and glial profiles. At least half of the dually labeled profiles were somata and dendrites, while most labeled axon terminals expressed only D2R‐ir. The D2R‐labeled terminals were without synaptic specializations or formed inhibitory or excitatory‐type synapses with somatodendritic profiles, some of which expressed the α7nAChR and/or D2R. Astrocytic glial processes comprised the majority of non‐somatodendritic α7nAChR or α7nAChR and D2R‐labeled profiles. Glial processes containing α7nAC...</description>
            <author>Synapse</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5147831</comments>
            <pubDate>Thu, 18 Aug 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5147831</guid>        </item>
        <item>
            <title>Periadolescent changes of D2‐AMPA interactions in the rat nucleus accumbens</title>
            <link>http://www.medworm.com/index.php?rid=5127009&amp;cid=s_33785_25_f&amp;fid=33785&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fsyn.20976</link>
            <description>AbstractMany aspects of dopamine systems mature during adolescence. In the nucleus accumbens, the modulation of prefrontal cortical synaptic responses by dopamine becomes refined during adolescence with the recruitment of a GABA component. As this GABA component is depolarizing, it remains to be determined whether this change affects action potential firing in nucleus accumbens neurons. Here we tested whether a D2 agonist affects AMPA‐evoked cell firing in slices containing the nucleus accumbens from juvenile (PD 28‐34) and adult (PD&amp;gt;60) rats. AMPA (0.1‐0.4 µM) depolarized nucleus accumbens neurons and increased their firing in a dose‐dependent manner. The D2 agonist quinpirole (2 µM) had different effects in juvenile vs. adult slices. In the juvenile accumbens, quinpirole enh...</description>
            <author>Synapse</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5127009</comments>
            <pubDate>Sun, 14 Aug 2011 05:51:16 +0100</pubDate>
            <guid isPermaLink="false">5127009</guid>        </item>
        <item>
            <title>Periadolescent changes of D2–AMPA interactions in the rat nucleus accumbens</title>
            <link>http://www.medworm.com/index.php?rid=5306014&amp;cid=s_33785_25_f&amp;fid=33785&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fsyn.20976</link>
            <description>AbstractMany aspects of dopamine (DA) systems mature during adolescence. In the nucleus accumbens, the modulation of prefrontal cortical synaptic responses by DA becomes refined during adolescence with the recruitment of a gamma‐amino butyric acid (GABA) component. As this GABA component is depolarizing, it remains to be determined whether this change affects action potential firing in nucleus accumbens neurons. Here we tested whether a D2 agonist affects AMPA‐evoked cell firing in slices containing the nucleus accumbens from juvenile (postnatal day, PD 28–34) and adult (PD &amp;gt; 60) rats. 2‐amino‐3‐(5‐methyl‐3‐oxo‐1,2‐oxazol‐4‐yl)propanoic acid (AMPA) (0.1–0.4 μM) depolarized nucleus accumbens neurons and increased their firing in a dose‐dependent manner. The...</description>
            <author>Synapse</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5306014</comments>
            <pubDate>Fri, 12 Aug 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5306014</guid>        </item>
        <item>
            <title>Heterogeneous voltage dependence of interneuron resonance in the hippocampal stratum radiatum of adult rats</title>
            <link>http://www.medworm.com/index.php?rid=5041790&amp;cid=s_33785_25_f&amp;fid=33785&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fsyn.20971</link>
            <description>(Source: Synapse)</description>
            <author>Synapse</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5041790</comments>
            <pubDate>Wed, 20 Jul 2011 21:16:49 +0100</pubDate>
            <guid isPermaLink="false">5041790</guid>        </item>
        <item>
            <title>Brain region‐selective cellular redistribution of mGlu5 but not GABAB receptors following methamphetamine‐induced associative learning</title>
            <link>http://www.medworm.com/index.php?rid=5041793&amp;cid=s_33785_25_f&amp;fid=33785&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fsyn.20968</link>
            <description>AbstractAlterations in receptor expression and distribution between cell surface and cytoplasm are means by which psychostimulants regulate neurotransmission. Metabotropic glutamate receptor subtype 5 (mGluR5) and GABAB receptors (GABABR) are critically involved in the development and expression of stimulant‐induced behaviors, including conditioned place preference (CPP), an index of drug‐seeking. However, it is not known if psychostimulant‐induced CPP alters the trafficking of these receptors. To fill this gap, the current study used methamphetamine (Meth)‐induced CPP in rats to ascertain if receptor changes occur in limbic brain regions that regulate drug‐seeking, the medial prefrontal cortex (mPFC), nucleus accumbens (NAc) and ventral pallidum (VP). To do so, ex vivo tissue wa...</description>
            <author>Synapse</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5041793</comments>
            <pubDate>Tue, 19 Jul 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5041793</guid>        </item>
        <item>
            <title>Donepezil, but not galantamine, blocks muscarinic receptor‐mediated in vitro and in vivo responses</title>
            <link>http://www.medworm.com/index.php?rid=5041792&amp;cid=s_33785_25_f&amp;fid=33785&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fsyn.20969</link>
            <description>AbstractWe have found that galantamine, but not donepezil, reversed isolation rearing‐induced deficits of prepulse inhibition (PPI) via an activation of muscarinic M1 receptors. To explain this difference, the present study examined the effects of these acetylcholinesterase inhibitors on muscarinic receptor‐mediated responses in in vitro and in vivo systems. Ca2+‐imaging study showed that donepezil, but not galantamine, blocked a muscarinic agonist carbachol‐induced increase in intracellular Ca2+ levels in SH‐SY5Y cells. Moreover, a microdialysis study showed that intraperitoneal administration of donepezil, but not galantamine, attenuated a preferential M1 receptor agonist N‐desmethylclozapine‐induced increase in dopamine release in mouse cerebral cortex. These results sugge...</description>
            <author>Synapse</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5041792</comments>
            <pubDate>Tue, 19 Jul 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5041792</guid>        </item>
        <item>
            <title>Imaging of dopamine D2/3 agonist binding in cocaine dependence: A [11C]NPA PET study</title>
            <link>http://www.medworm.com/index.php?rid=5041791&amp;cid=s_33785_25_f&amp;fid=33785&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fsyn.20970</link>
            <description>Conclusions:The results of this [11C]NPA PET study do not support alterations in D2/3 HIGH binding in the striatum in cocaine dependence. Synapse, 2011. © 2011 Wiley‐Liss, Inc. (Source: Synapse)</description>
            <author>Synapse</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5041791</comments>
            <pubDate>Tue, 19 Jul 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5041791</guid>        </item>
        <item>
            <title>Methamphetamine‐mediated modulation of MOR expression in the SH‐SY5Y neuroblastoma cell line</title>
            <link>http://www.medworm.com/index.php?rid=5001179&amp;cid=s_33785_25_f&amp;fid=33785&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fsyn.20913</link>
            <description>AbstractMethamphetamine (METH) has been shown to induce oxidative stress in SH‐SY5Y cells, a neuroblastic, dopaminergic cell line model. In neuronal cells, oxidation of dopamine by auto‐oxidative or enzymatic mechanisms leads to the production of reactive oxygen species (ROS). Neuronal cells treated with METH accumulate dopamine, which can ultimately lead to increased levels of ROS. ROS has been shown to mediate the expression of the mu‐opioid receptor (MOR). The goal of this in vitro study was to examine the effects of METH on the accumulation of intracellular ROS in SH‐SY5Y cells, which could, in turn, modulate MOR expression. Confocal laser scanning microscopy (CLSM) indicated that METH induced intracellular accumulation of ROS, detected as increased fluorescence of rhodamine 12...</description>
            <author>Synapse</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5001179</comments>
            <pubDate>Thu, 07 Jul 2011 14:12:57 +0100</pubDate>
            <guid isPermaLink="false">5001179</guid>        </item>
        <item>
            <title>Phenotypic disruption to orofacial movement topography in conditional mutants with generalized CamKIIa/Cre D1Tox versus striatal‐specific DARPP‐32/Cre D1Tox ablation of D1 dopamine receptor‐expressing cells</title>
            <link>http://www.medworm.com/index.php?rid=5001178&amp;cid=s_33785_25_f&amp;fid=33785&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fsyn.20910</link>
            <description>AbstractOrofacial movements were quantified in (a) DARPP‐32/Cre D1Tox mutants, having progressive loss of D1 dopamine receptor expressing striatal medium spiny neurons and (b) CamKIIa/Cre D1Tox mutants, having progressive, generalized loss of forebrain D1 receptor expressing cells. Horizontal jaw movements and tongue protrusions were reduced in DARPP‐32/Cre but not in CamKIIa/Cre mutants; head and vibrissae movements were increased in DARPP‐32/Cre but decreased in CamKIIa/Cre mutants. In drug challenge studies, tongue protrusions were increased in CamKIIa/Cre mutants following vehicle, suggesting a stress‐related phenotype. These findings indicate that mice with progressive loss of striatal‐specific D1 receptor expressing cells have an orofacial phenotype that may be modulated by...</description>
            <author>Synapse</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5001178</comments>
            <pubDate>Thu, 07 Jul 2011 14:12:56 +0100</pubDate>
            <guid isPermaLink="false">5001178</guid>        </item>
        <item>
            <title>Announcement</title>
            <link>http://www.medworm.com/index.php?rid=5001177&amp;cid=s_33785_25_f&amp;fid=33785&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fsyn.20967</link>
            <description>AbstractAfter 25 years as Editor‐in‐Chief of Synapse, I will be retiring from the journal as of January 1, 2012. I founded this journal in 1987, and it has been a very enjoyable experience. Wiley will be organizing a search committee to find the appropriate replacement. I wish Synapse all the best for the future. (Source: Synapse)</description>
            <author>Synapse</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5001177</comments>
            <pubDate>Thu, 07 Jul 2011 14:12:55 +0100</pubDate>
            <guid isPermaLink="false">5001177</guid>        </item>
        <item>
            <title>Translational characterization of [11C]GSK931145, a PET ligand for the glycine transporter type 1 (GlyT‐1)</title>
            <link>http://www.medworm.com/index.php?rid=4939879&amp;cid=s_33785_25_f&amp;fid=33785&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fsyn.20966</link>
            <description>We report on [11C]GSK931145 as a novel GlyT‐1 imaging probe in primate and man. Primate PET studies were performed to determine the level of specific binding following homologous competition with GSK931145 and the plasma‐occupancy relationship of the GlyT‐1 inhibitor GSK1018921. Human PET studies were performed to determine the test‐retest reproducibility of [11C]GSK931145 and the plasma‐occupancy relationship of GSK1018921. [11C]GSK931145 entered primate and human brain and yielded a heterogeneous pattern of uptake which was similar in both species with highest uptake in midbrain, thalamus and cerebellum. Homologous competition in primates indicated no viable reference region and gave binding potential estimates between 1.5‐3 for midbrain, thalamus and cerebellum, Whilst the d...</description>
            <author>Synapse</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4939879</comments>
            <pubDate>Sat, 18 Jun 2011 20:07:10 +0100</pubDate>
            <guid isPermaLink="false">4939879</guid>        </item>
        <item>
            <title>Translational characterization of [11C]GSK931145, a PET ligand for the glycine transporter type 1</title>
            <link>http://www.medworm.com/index.php?rid=5127010&amp;cid=s_33785_25_f&amp;fid=33785&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fsyn.20966</link>
            <description>We report on [11C]GSK931145 as a novel GlyT‐1 imaging probe in primate and man. Primate PET studies were performed to determine the level of specific binding following homologous competition with GSK931145 and the plasma‐occupancy relationship of the GlyT‐1 inhibitor GSK1018921. Human PET studies were performed to determine the test–retest reproducibility of [11C]GSK931145 and the plasma‐occupancy relationship of GSK1018921. [11C]GSK931145 entered primate and human brain and yielded a heterogeneous pattern of uptake which was similar in both species with highest uptake in midbrain, thalamus, and cerebellum. Homologous competition in primates indicated no viable reference region and gave binding potential estimates between 1.5 and 3 for midbrain, thalamus and cerebellum, While the...</description>
            <author>Synapse</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5127010</comments>
            <pubDate>Thu, 16 Jun 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5127010</guid>        </item>
        <item>
            <title>Specific α4β2 nicotinic acetylcholine receptor binding of [F‐18]nifene in the rhesus monkey</title>
            <link>http://www.medworm.com/index.php?rid=4939880&amp;cid=s_33785_25_f&amp;fid=33785&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fsyn.20965</link>
            <description>Conclusions: [F‐18]Nifene exhibits rapid equilibration and a moderately high target to background binding profile in the α4β2* nAChR rich regions of the brain, thus providing favorable imaging characteristics as a PET radiotracer for nAChR assay. Synapse, 2011. © 2011 Wiley‐Liss, Inc. (Source: Synapse)</description>
            <author>Synapse</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4939880</comments>
            <pubDate>Mon, 13 Jun 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4939880</guid>        </item>
        <item>
            <title>Attenuation of inhibitory synaptic transmission by glial dysfunction in rat thalamus</title>
            <link>http://www.medworm.com/index.php?rid=4905875&amp;cid=s_33785_25_f&amp;fid=33785&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fsyn.20964</link>
            <description>AbstractThe thalamus serves as the obligatory gateway to the neocortex for sensory processing, and also serves as a pathway for corticocortical communication. In addition, the reciprocal synaptic connectivity between the thalamic reticular nucleus (TRN) and adjacent thalamic relay nuclei generates rhythmic activities similar to that observed during different arousal states and certain neurological conditions such as absence epilepsy. Epileptiform activity can arise from a variety of neural mechanisms, but in addition glia are thought to have an important role in such activities as well. Glia serve a central role in glutamine synthesis, a precursor for glutamate or GABA in nerve terminals. While alterations in glutamine shuttling from glia to neurons can influence GABA and glutamate neurotr...</description>
            <author>Synapse</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4905875</comments>
            <pubDate>Wed, 08 Jun 2011 14:19:53 +0100</pubDate>
            <guid isPermaLink="false">4905875</guid>        </item>
        <item>
            <title>The Gray area between synapse structure and function—Gray's synapse types I and II revisited</title>
            <link>http://www.medworm.com/index.php?rid=4939882&amp;cid=s_33785_25_f&amp;fid=33785&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fsyn.20962</link>
            <description>AbstractOn the basis of ultrastructural parameters, the concept was formulated that asymmetric Type I and symmetric Type II synapses are excitatory and inhibitory, respectively. This “functional Gray synapses concept” received strong support from the demonstration of the excitatory neurotransmitter glutamate in Type I synapses and of the inhibitory neurotransmitter γ‐aminobutyric acid in Type II synapses, and is still frequently used in modern literature. However, morphological and functional evidence has accumulated that the concept is less tenable. Typical features of synapses like shape and size of presynaptic vesicles and synaptic cleft and presence of a postsynaptic density (PsD) do not always fit the postulated (excitatory/inhibitory) function of Gray's synapses. Furthermore, ...</description>
            <author>Synapse</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4939882</comments>
            <pubDate>Mon, 06 Jun 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4939882</guid>        </item>
        <item>
            <title>The gray area between synapse structure and function – Gray's synapse types I and II revisited</title>
            <link>http://www.medworm.com/index.php?rid=4905877&amp;cid=s_33785_25_f&amp;fid=33785&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fsyn.20962</link>
            <description>AbstractOn the basis of ultrastructural parameters, the concept was formulated that asymmetric type I and symmetric type II synapses are excitatory and inhibitory, respectively. This “functional Gray synapses concept” received strong support from the demonstration of the excitatory neurotransmitter glutamate in type I synapses and of the inhibitory neurotransmitter γ‐aminobutyric acid in type II synapses, and is still frequently used in modern literature. However, morphological and functional evidence has accumulated that the concept is less tenable. Typical features of synapses like shape and size of presynaptic vesicles and synaptic cleft and presence of a postsynaptic density (PsD), do not always fit the postulated (excitatory/inhibitory) function of Gray's synapses. Furthermore,...</description>
            <author>Synapse</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4905877</comments>
            <pubDate>Mon, 06 Jun 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4905877</guid>        </item>
        <item>
            <title>Glycine receptor internalization by protein kinases activation</title>
            <link>http://www.medworm.com/index.php?rid=4905876&amp;cid=s_33785_25_f&amp;fid=33785&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fsyn.20963</link>
            <description>AbstractAlthough glycine‐induced currents in the central nervous system have been proven to be modulated by protein kinases A (PKA) and C (PKC), the mechanism is not well understood. In order to better comprehend the mechanism involved in this phenomenon, we tested the PKA and PKC activation effect on the specific [3H]glycine and [3H]strychnine binding to post‐synaptic glycine receptor (GlyR) in intact rat retina. The specific binding constituted about 20% of the total radioligand binding. Kinetic analysis of the specific binding exhibited a sigmoidal behavior with three glycine and two strychnine binding sites and affinities of 212 nM for [3H]glycine and 50 nM for [3H]strychnine. Specific radioligand binding was decreased (60‐85%) by PKA and PKC activation, an effect that was blocke...</description>
            <author>Synapse</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4905876</comments>
            <pubDate>Mon, 06 Jun 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4905876</guid>        </item>
        <item>
            <title>Erratum: Kovačević et al., Chronic fluoxetine treatment has a larger effect on the density of a serotonin transporter in the FSL rat model of depression than in normal rats</title>
            <link>http://www.medworm.com/index.php?rid=4886968&amp;cid=s_33785_25_f&amp;fid=33785&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fsyn.20940</link>
            <description>(Source: Synapse)</description>
            <author>Synapse</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4886968</comments>
            <pubDate>Thu, 02 Jun 2011 18:21:55 +0100</pubDate>
            <guid isPermaLink="false">4886968</guid>        </item>
        <item>
            <title>Expression pattern of Mical‐1 in the temporal neocortex of patients with intractable temporal epilepsy and Pilocarpine‐induced rat model</title>
            <link>http://www.medworm.com/index.php?rid=4886962&amp;cid=s_33785_25_f&amp;fid=33785&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fsyn.20961</link>
            <description>AbstractMical‐1 is a novel F‐actin‐disassembly factor that is critical in actin reorganization. It provides a molecular conduit through which actin reorganizes‐a hallmark of cell morphological changes, including axon navigation. However, whether Mical‐1 is involved in the epileptogenesis remains unknown. Here, we investigate Mical‐1 expression pattern in intractable temporal lobe epilepsy (TLE) patients and Pilocarpine‐induced rat model. We used double‐labled immunoflurescence, immunohistochemistry and western blotting to assess the location and expression of Mical‐1 in temporal neocortex of intractable TLE patients, and the expression pattern of Mical‐1 at different time point in the hippocampus and temporal lobe cortex of the Pilocarpine‐induced rat model. Double‐...</description>
            <author>Synapse</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4886962</comments>
            <pubDate>Thu, 02 Jun 2011 18:21:14 +0100</pubDate>
            <guid isPermaLink="false">4886962</guid>        </item>
        <item>
            <title>Changes in dynorphin immunoreactivity but unaltered density of enkephalin immunoreactive neurons in basal ganglia nuclei of genetically dystonic hamsters</title>
            <link>http://www.medworm.com/index.php?rid=4886964&amp;cid=s_33785_25_f&amp;fid=33785&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fsyn.20959</link>
            <description>AbstractDystonia is regarded as a basal ganglia disorder. In the dtsz hamster, a genetic animal model of paroxysmal dystonia, previous studies demonstrated a reduced density of striatal GABAergic interneurons which inhibit striatal GABAergic projection neurons. Although the disinhibition of striatal GABAergic projection neurons was evidenced in the dtsz hamster, alterations in their density have not been elucidated so far.Therefore, in the present study, the density of striatal methionin‐(met‐) enkephalin (ENK) immunoreactive GABAergic neurons, which project to the globus pallidus (indirect pathway), was determined in dtsz and control hamsters to clarify a possible role of an altered ratio between striatal interneurons and projection neurons. Furthermore, the immunoreactivity of dynorp...</description>
            <author>Synapse</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4886964</comments>
            <pubDate>Wed, 01 Jun 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4886964</guid>        </item>
        <item>
            <title>Connecting the dots of the cerebro‐cerebellar role in cognitive function: Neuronal pathways for cerebellar modulation of dopamine release in the prefrontal cortex</title>
            <link>http://www.medworm.com/index.php?rid=4886963&amp;cid=s_33785_25_f&amp;fid=33785&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fsyn.20960</link>
            <description>AbstractCerebellar involvement in autism, schizophrenia and other cognitive disorders, is typically associated with prefrontal cortical pathology. However, the underlying neuronal mechanisms are largely unknown. It has previously been shown in mice that stimulation of the dentate nucleus of the cerebellum (DN) evokes dopamine release in the medial prefrontal cortex (mPFC). Here we investigated the neuronal circuitry by which the cerebellum modulates mPFC dopamine release. Fixed potential amperometry was used to determine the contribution of two candidate pathways by which the cerebellum may modulate mPFC dopamine release. In urethane anesthetized mice, dopamine release evoked by DN stimulation (100 Hz) was recorded in mPFC following local anesthetic lidocaine (0.02 µg) or ionotropic gluta...</description>
            <author>Synapse</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4886963</comments>
            <pubDate>Wed, 01 Jun 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4886963</guid>        </item>
        <item>
            <title>Chronically saturating levels of endogenous glycine disrupt glutamatergic neurotransmission and enhance synaptogenesis in the CA1 region of mouse hippocampus</title>
            <link>http://www.medworm.com/index.php?rid=4886967&amp;cid=s_33785_25_f&amp;fid=33785&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fsyn.20956</link>
            <description>AbstractGlycine serves a dual role in neurotransmission. It is the primary inhibitory neurotransmitter in the spinal cord and brain stem and is also an obligatory co‐agonist at the excitatory glutamate, N‐methyl‐D‐aspartate receptor (NMDAR). Therefore, the postsynaptic action of glycine should be strongly regulated to maintain a balance between its inhibitory and excitatory inputs. The glycine concentration at the synapse is tightly regulated by 2 types of glycine transporters, GlyT1 and GlyT2, located on nerve terminals or astrocytes. Genetic studies demonstrated that homozygous (GlyT1‐/‐) newborn mice display severe sensorimotor deficits characterized by lethargy, hypotonia and hyporesponsivity to tactile stimuli and ultimately die in their first post‐natal day. These sympt...</description>
            <author>Synapse</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4886967</comments>
            <pubDate>Tue, 31 May 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4886967</guid>        </item>
        <item>
            <title>Alzheimer's disease: β‐amyloid plaque formation in human brain</title>
            <link>http://www.medworm.com/index.php?rid=4886966&amp;cid=s_33785_25_f&amp;fid=33785&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fsyn.20957</link>
            <description>AbstractAlthough the precise cause of Alzheimer's disease is not known, the β‐amyloid peptide chains of 40 to 42 amino acids are suspected to contribute to the disease. The β‐amyloid precursor protein is found on many types of cell membranes, and the action of secretases (β and γ) on this precursor protein normally releases the β‐amyloids at a high rate into the plasma and the cerebrospinal fluid. However, the concentrations of the β‐amyloids in the plasma and the spinal fluid vary considerably between laboratories. The β‐amyloids adsorb in the nM concentration range to receptors on neuronal and glial cells. The β‐amyloids are internalized, become folded in the β‐folded or β‐pleated shape, and then stack upon each other to form long fibrils and aggregates known as...</description>
            <author>Synapse</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4886966</comments>
            <pubDate>Tue, 31 May 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4886966</guid>        </item>
        <item>
            <title>Identifying the serotonin transporter signal in western blot studies of the neurotoxic potential of MDMA and related drugs</title>
            <link>http://www.medworm.com/index.php?rid=4886965&amp;cid=s_33785_25_f&amp;fid=33785&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fsyn.20958</link>
            <description>AbstractA number of published studies have questioned the serotonin neurotoxic potential of 3,4‐methylenedioxymethamphetamine (MDMA, “ecstasy”) and related drugs (fenfluramine, p‐chloroamphetamine) based upon results from Western blot studies with a custom synthesized serotonin transporter (SERT) antibody that found no reduction in the abundance of the SERT protein after substituted amphetamine treatment. The purpose of the present study was to collect Western blot data using the same SERT antibody used in those studies, but with positive and negative controls. A 63‐68 kDa band that had the regional distribution expected of rat brain SERT, was decreased by 5,7‐DHT, and was absent in SERT KO animal was identified as the SERT signal. Significant, lasting decreases in the abundanc...</description>
            <author>Synapse</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4886965</comments>
            <pubDate>Tue, 31 May 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4886965</guid>        </item>
        <item>
            <title>Impact of isoflurane anesthesia on D2 receptor 1 occupancy by [18F]fallypride measured by microPET with a modified Logan plot</title>
            <link>http://www.medworm.com/index.php?rid=4833517&amp;cid=s_33785_25_f&amp;fid=33785&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fsyn.20955</link>
            <description>Conclusion: The results of this study demonstrate that isoflurane anesthesia significantly decreases striatal [18F]fallypride BPND in rats. Of similar importance, this work demonstrates the effectiveness of delayed scans following radiotracer injection and the implication that different types of studies can be conducted simultaneously with this method, including studies of behavioral and environmental impact on brain receptors. Synapse, 2011. © 2011 Wiley‐Liss, Inc. (Source: Synapse)</description>
            <author>Synapse</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4833517</comments>
            <pubDate>Wed, 18 May 2011 21:23:04 +0100</pubDate>
            <guid isPermaLink="false">4833517</guid>        </item>
        <item>
            <title>Impact of isoflurane anesthesia on D2 receptor occupancy by [18F]fallypride measured by microPET with a modified Logan plot</title>
            <link>http://www.medworm.com/index.php?rid=4939881&amp;cid=s_33785_25_f&amp;fid=33785&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fsyn.20955</link>
            <description>Conclusion: The results of this study demonstrate that isoflurane anesthesia significantly decreases striatal [18F]fallypride BPND in rats. Of similar importance, this work demonstrates the effectiveness of delayed scans following radiotracer injection and the implication that different types of studies can be conducted simultaneously with this method, including studies of behavioral and environmental impact on brain receptors. Synapse, 2011. © 2011 Wiley‐Liss, Inc. (Source: Synapse)</description>
            <author>Synapse</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4939881</comments>
            <pubDate>Sun, 15 May 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4939881</guid>        </item>
        <item>
            <title>Requirement of α7 nicotinic acetylcholine receptors for amyloid beta protein‐induced depression of hippocampal long‐term potentiation in CA1 region of rats in vivo</title>
            <link>http://www.medworm.com/index.php?rid=4915534&amp;cid=s_33785_25_f&amp;fid=33785&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fsyn.20951</link>
            <description>This study examined the effects of different Aβ fragments on hippocampal long‐term potentiation (LTP) and investigated its probable α7 nicotinic acetylcholine receptors (nAChRs) mechanism. The results show that: (1) intracerebroventicular injection of Aβ25–35 or Aβ31–35 significantly and similarly suppressed hippocampal LTP in CA1 region in rats; (2) choline, a selective α7 nAChR agonist, did not affect the LTP induction but enhanced LTP suppression induced by Aβ31–35; and (3) methyllycaconitine, a specific α7 nAChR antagonist, slightly suppressed hippocamal LTP but effectively prevented against Aβ31–35‐induced LTP depression in the presence of Aβ31–35. These results indicate that: (1) the amino acid sequence 31–35 of the Aβ peptide might be a shorter active seque...</description>
            <author>Synapse</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4915534</comments>
            <pubDate>Sun, 15 May 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4915534</guid>        </item>
        <item>
            <title>Inhibition of the serotonin transporter induces microglial activation and downregulation of dopaminergic neurons in the substantia nigra</title>
            <link>http://www.medworm.com/index.php?rid=4833521&amp;cid=s_33785_25_f&amp;fid=33785&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fsyn.20954</link>
            <description>AbstractDrugs that selectively inhibit the serotonin transporter (SERT) are widely used in the treatment of depression and anxiety disorders. These agents are associated with a range of extrapyramidal syndromes such as akathisia, dystonia, dyskinesia and parkinsonism, suggesting an effect on dopaminergic transmission. We studied the time course of changes in dopaminergic neurons in the substantia nigra (SN) after initiation of two different SERT inhibitors, citalopram and fluoxetine. In the first experiment, groups of Sprague‐Dawley rats received daily meals of rice pudding either alone (N=9) or mixed with citalopram 5 mg/kg/day (N=27). Rats were sacrificed after 24 hours, 7 days or 28 days of treatment. Sections of SN were processed for tyrosine hydroxylase (TH) immunohistochemistry. Ci...</description>
            <author>Synapse</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4833521</comments>
            <pubDate>Sun, 15 May 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4833521</guid>        </item>
        <item>
            <title>α7 nicotinic acetylcholine receptors are required for Aβ‐induced depression of hippocampal LTP in CA1 region of rats in vivo</title>
            <link>http://www.medworm.com/index.php?rid=4833520&amp;cid=s_33785_25_f&amp;fid=33785&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fsyn.20951</link>
            <description>AbstractThe high density of senile plaques with β‐amyloid peptide (Aβ) and the cholinergic neuron loss in the brain are the dominated pathological characteristics of Alzheimer's disease (AD). However, the active center of Aβ, especially the cholinergic mechanism underlying the Aβ neurotoxicity, is mostly unknown. The present study examined the effects of different Aβ fragments on hippocampal LTP and investigated its probable α7 nAChRs mechanism. The results show that: (1) intracerebroventicular injection of Aβ25‐35 or Aβ31‐35 significantly and similarly suppressed hippocampal LTP in CA1 region in rats; (2) choline, a selective α7 nAChR agonist, did not affect the LTP induction, but enhanced LTP suppression induced by Aβ31‐35; (3) Methyllycaconitine (MLA), a specific α7 n...</description>
            <author>Synapse</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4833520</comments>
            <pubDate>Sun, 15 May 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4833520</guid>        </item>
        <item>
            <title>Involvement of NMDA receptors in ryanodine receptor expression in dopaminergic neurons in the ventral tegmental area of mice with intermittent methamphetamine treatment</title>
            <link>http://www.medworm.com/index.php?rid=4833519&amp;cid=s_33785_25_f&amp;fid=33785&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fsyn.20953</link>
            <description>AbstractExcitatory synapses on dopaminergic neurons of the ventral tegmental area (VTA) represent an important role in psychostimulant‐induced rewarding effect. The present study investigated the regulation of ryanodine receptor (RyR) and NMDA receptor expression in mice under intermittent methamphetamine (METH) treatment using a place preference procedure. RyR‐1 and ‐2 significantly increased in the VTA of mice with METH‐induced place preference, whereas RyR‐3 showed no changes. In addition, the levels of NR1, NR2A and NR2B subunits were increased in the VTA. The METH‐induced place preference was inhibited by intracerebroventricular pretreatment with MK‐801, a non‐competitive NMDA receptor antagonist, and ifenprodil, a selective NR2B subunit‐containing NMDA receptor anta...</description>
            <author>Synapse</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4833519</comments>
            <pubDate>Sun, 15 May 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4833519</guid>        </item>
        <item>
            <title>Striatal dopamine D1 and D2 receptors: Widespread influences on methamphetamine‐induced dopamine and serotonin neurotoxicity</title>
            <link>http://www.medworm.com/index.php?rid=4833518&amp;cid=s_33785_25_f&amp;fid=33785&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fsyn.20952</link>
            <description>This study demonstrates that (1) dopamine D1 and D2 receptors in striatum, like nigral D1 receptors, are needed for mAMPH‐induced striatal DAT reductions, (2) these same receptors are needed for mAMPH‐induced SERT loss, and (3) these widespread influences of striatal dopamine receptor antagonists are likely attributable to circuits connecting basal ganglia to thalamus and cortex. Synapse, 2011. © 2011 Wiley‐Liss, Inc. (Source: Synapse)</description>
            <author>Synapse</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4833518</comments>
            <pubDate>Sun, 15 May 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4833518</guid>        </item>
        <item>
            <title>The chronic administration of cerebrolysin induces plastic changes in the prefrontal cortex and dentate gyrus in aged mice</title>
            <link>http://www.medworm.com/index.php?rid=4784130&amp;cid=s_33785_25_f&amp;fid=33785&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fsyn.20950</link>
            <description>AbstractCerebrolysin (Cbl) is a mixture of neuropeptides with effects similar to the endogenous neurotrophic factors and is considered one of the best drugs used in the treatment of dementias such as Alzheimer's disease (AD). In brains with AD, morphological changes in the dendrites of pyramidal neurons of the prefrontal cortex (PFC) and hippocampus have been reported. These changes are reflected particularly in the decrement of both the dendritic tree and spine density. Here we evaluated the effect of this drug on the dendrites of pyramidal neurons of the PFC and CA1 dorsal hippocampus and granule cells from the dentate gyrus (DG) and medium spiny neurons of the nucleus accumbens (NAcc) of aged mice. Cbl (5 ml/kg, i.p.) was administered daily for 60 days to 6‐month‐old mice. Dendritic...</description>
            <author>Synapse</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4784130</comments>
            <pubDate>Thu, 05 May 2011 19:20:13 +0100</pubDate>
            <guid isPermaLink="false">4784130</guid>        </item>
        <item>
            <title>Enhancement of histone acetylation in midbrain of mice with ethanol physical dependence and its withdrawal</title>
            <link>http://www.medworm.com/index.php?rid=4769025&amp;cid=s_33785_25_f&amp;fid=33785&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fsyn.20947</link>
            <description>AbstractThe present study investigated changes in histone acetylation in the midbrain including the ventral tegmental area in ethanol‐dependent and –withdrawn mice. Phospho‐CREB (p‐CREB), calcium/calmodulin dependent kinase IV (CaMKIV) and acetylated histone H3 (Ac‐H3) were up‐regulated in mice with ethanol physical dependence. Moreover, the up‐regulation of these proteins also increased 10 hr and 3 days after withdrawal from ethanol. Enhanced Ac‐H3 changed synaptic plasticity genes including BDNF, neurexin, SVP, PSD95, GluR1, NR2B, CaMKII, CREB, Cdk5 promoters in the conditions with ethanol physical dependence, increased synaptic plasticity genes including BDNF, Homer1, Fos, neurexin, SVP, PSD95, GluR1, NR2A, NR2B, CaMKII, CREB, Cdk5 promoters 10 hr after ethanol withdrawa...</description>
            <author>Synapse</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4769025</comments>
            <pubDate>Sun, 01 May 2011 16:23:37 +0100</pubDate>
            <guid isPermaLink="false">4769025</guid>        </item>
        <item>
            <title>Characterization of in vivo pharmacological properties and sensitivity to endogenous serotonin of [11C] P943: A positron emission tomography study in Papio anubis</title>
            <link>http://www.medworm.com/index.php?rid=4844054&amp;cid=s_33785_25_f&amp;fid=33785&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fsyn.20946</link>
            <description>Abstract[11C] P943 is a recently developed PET radiotracer for serotonin 5‐HT1B receptors. We characterized a number of its in vivo pharmacokinetic properties, including the evaluation of its two stereo‐isomers, saturability of specific binding, selectivity for 5‐HT1B and 5‐HT1D receptors, and vulnerability to pharmacologically induced increases in endogenous 5‐HT levels. Six isoflurane‐anesthetized baboons were scanned with [11C] P943 at baseline, and following various pharmacological manipulations. The interventions included the administration of pharmacological doses of P943, SB‐616234‐S (a 5‐HT1B selective antagonist), SB‐714786 (a 5‐HT1D selective antagonist), as well as the administration of 5‐HT releasing agents (fenfluramine, amphetamine) and 5‐HT reuptake...</description>
            <author>Synapse</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4844054</comments>
            <pubDate>Thu, 28 Apr 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4844054</guid>        </item>
        <item>
            <title>Recombinant human immunodeficiency virus‐1 transactivator of transcription1–86 allosterically modulates dopamine transporter activity</title>
            <link>http://www.medworm.com/index.php?rid=4833522&amp;cid=s_33785_25_f&amp;fid=33785&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fsyn.20949</link>
            <description>(Source: Synapse)</description>
            <author>Synapse</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4833522</comments>
            <pubDate>Thu, 28 Apr 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4833522</guid>        </item>
        <item>
            <title>Characterisation of in vivo pharmacological properties and sensitivity to endogenous serotonin of [11C] P943: a positron emission tomography study in Papio Anubis</title>
            <link>http://www.medworm.com/index.php?rid=4769028&amp;cid=s_33785_25_f&amp;fid=33785&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fsyn.20946</link>
            <description>Abstract[11C] P943 is a recently developed PET radiotracer for serotonin 5‐HT1B receptors. We characterized a number of its in vivo pharmacokinetic properties, including the evaluation of its two stereo‐isomers, saturability of specific binding, selectivity for 5‐HT1B and 5‐HT1D receptors and vulnerability to pharmacologically induced increases in endogenous 5‐HT levels. Six isoflurane‐anesthetized baboons were scanned with [11C] P943 at baseline, and following various pharmacological manipulations. The interventions included the administration of pharmacological doses of P943, SB‐616234‐S (a 5‐HT1B selective antagonist), SB‐714786 (a 5‐HT1D selective antagonist), as well as the administration of 5‐HT releasing agents (fenfluramine, amphetamine) and 5‐HT reuptake ...</description>
            <author>Synapse</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4769028</comments>
            <pubDate>Thu, 28 Apr 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4769028</guid>        </item>
        <item>
            <title>Motor activity affects dopaminergic and noradrenergic systems of the dorsal horn of the rat lumbar spinal cord</title>
            <link>http://www.medworm.com/index.php?rid=4769027&amp;cid=s_33785_25_f&amp;fid=33785&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fsyn.20948</link>
            <description>AbstractDopamine (DA) and noradrenaline (NA) modulate responses to nociceptive stimuli, within the dorsal horn of the spinal cord. Both neurotransmitters may play a role in supra‐spinal regulation or response to proprioceptive afferences to the dorsal horn.However, direct evidence of changes in neurotransmitter release within the dorsal horn due to non‐noxious stimuli is lacking.The present study was designed to determine, whether non‐nociceptive exercise produces changes in release of DA and NA within the dorsal horn and, whether these changes are associated with long‐lasting inhibition after the exercise stops.Microdialysis probes, implanted in layers 2‐5 of Rexed, in combination with HPLC‐EC were used to measure concentrations of DA and NA metabolite 3‐methoxy‐4‐hydrox...</description>
            <author>Synapse</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4769027</comments>
            <pubDate>Thu, 28 Apr 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4769027</guid>        </item>
        <item>
            <title>Recombinant HIV‐1TAT1‐86 allosterically modulates dopamine transporter activity</title>
            <link>http://www.medworm.com/index.php?rid=4769026&amp;cid=s_33785_25_f&amp;fid=33785&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fsyn.20949</link>
            <description>(Source: Synapse)</description>
            <author>Synapse</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4769026</comments>
            <pubDate>Thu, 28 Apr 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4769026</guid>        </item>
        <item>
            <title>Growth hormone (GH) increases neural cell adhesion (NCAM) polysialylation state in the dentate gyrus of gamma irradiated rats</title>
            <link>http://www.medworm.com/index.php?rid=4759952&amp;cid=s_33785_25_f&amp;fid=33785&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fsyn.20945</link>
            <description>(Source: Synapse)</description>
            <author>Synapse</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4759952</comments>
            <pubDate>Thu, 28 Apr 2011 17:44:00 +0100</pubDate>
            <guid isPermaLink="false">4759952</guid>        </item>
        <item>
            <title>D‐cycloserine facilitates extinction of cocaine self administration in c57 mice</title>
            <link>http://www.medworm.com/index.php?rid=4727394&amp;cid=s_33785_25_f&amp;fid=33785&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fsyn.20944</link>
            <description>Conclusion:DCS accelerated extinction with the presence of cues, but there were no differences on extinction without cues as compared with vehicle. These findings are consistent with DCS disrupting the memory process associated with the cues. Since drug cues are significantly involved in relapse, these findings support research to assess the therapeutic potential of DCS in cocaine addiction. Synapse, 2011. © 2011 Wiley‐Liss, Inc. (Source: Synapse)</description>
            <author>Synapse</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4727394</comments>
            <pubDate>Wed, 20 Apr 2011 03:41:54 +0100</pubDate>
            <guid isPermaLink="false">4727394</guid>        </item>
        <item>
            <title>D‐cycloserine facilitates extinction of cocaine self‐administration in c57 mice</title>
            <link>http://www.medworm.com/index.php?rid=4833524&amp;cid=s_33785_25_f&amp;fid=33785&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fsyn.20944</link>
            <description>Conclusion: DCS accelerated extinction with the presence of cues, but there were no differences on extinction without cues as compared with vehicle. These findings are consistent with DCS disrupting the memory process associated with the cues. Since drug cues are significantly involved in relapse, these findings support research to assess the therapeutic potential of DCS in cocaine addiction. Synapse 2011. © 2011 Wiley‐Liss, Inc. (Source: Synapse)</description>
            <author>Synapse</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4833524</comments>
            <pubDate>Mon, 18 Apr 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4833524</guid>        </item>
        <item>
            <title>Attenuated methamphetamine induced neurotoxicity by modafinil administration in mice</title>
            <link>http://www.medworm.com/index.php?rid=4727395&amp;cid=s_33785_25_f&amp;fid=33785&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fsyn.20943</link>
            <description>In this study we tested possible neuroprotective effects of modafinil after toxic METH administration in mice. We evaluated the effect of modafinil (2 injections of either 90 or 180 mg/kg) and METH binge (3x7 mg/kg i.p. injections, 3h apart) co‐administration on dopamine striatal content, TH immunoreactivity in striatal areas and spontaneous locomotor activity. We also investigated acute locomotor activity and stereotypy profile in mice treated with a single METH dose (2 and 7mg/kg) pre‐treated with modafinil (90 and 180 mg/kg). We found that mice treated with a METH binge showed a marked decrease in DA and dopaminergic metabolites as well as lower levels of TH immunoreactivity in the dorsal striatum. Pre‐treatment with modafinil (both 90 and 180mg/kg) attenuated these effects but di...</description>
            <author>Synapse</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4727395</comments>
            <pubDate>Mon, 18 Apr 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4727395</guid>        </item>
        <item>
            <title>Assessing the sensitivity of [11C]P943, a novel 5‐HTIB PET radioligand, to endogenous serotonin release</title>
            <link>http://www.medworm.com/index.php?rid=4699640&amp;cid=s_33785_25_f&amp;fid=33785&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fsyn.20942</link>
            <description>AbstractThe main objective of the current study was to determine the sensitivity of the PET radioligand [11C]P943 to fenfluramine‐induced changes in endogenous 5‐HT in nonhuman primate brain. Fenfluramine‐induced changes in 5‐HT1B occupancy were compared to those obtained by self‐block with unlabeled P943. Two baboons and 1 rhesus monkey were given preblocking or displacing doses of fenfluramine (1‐5 mg/kg) or preblocking doses of unlabeled P943 (0.2 mg/kg) and imaged with [11C]P943 PET. Receptor occupancy by the low dose of fenfluramine (1 mg/kg) in the baboons was 25% and 29% and by the high dose of fenfluramine (5 mg/kg) in the rhesus macaque was 42%. Receptor occupancy by P943 (0.2 mg/kg) was 68% and 86% in the baboons. PET imaging of 5‐HT1B receptors with [11C]P943 may b...</description>
            <author>Synapse</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4699640</comments>
            <pubDate>Tue, 12 Apr 2011 18:58:17 +0100</pubDate>
            <guid isPermaLink="false">4699640</guid>        </item>
        <item>
            <title>Assessing the sensitivity of [11C]p943, a novel 5‐HTIB radioligand, to endogenous serotonin release</title>
            <link>http://www.medworm.com/index.php?rid=4784133&amp;cid=s_33785_25_f&amp;fid=33785&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fsyn.20942</link>
            <description>AbstractThe main objective of the current study was to determine the sensitivity of the positron emission tomography (PET) radioligand [11C]P943 to fenfluramine‐induced changes in endogenous 5‐HT in nonhuman primate brain. Fenfluramine‐induced changes in 5‐HT1B occupancy were compared to those obtained by self‐block with unlabeled P943. Two baboons and 1 rhesus monkey were given preblocking or displacing doses of fenfluramine (1–5 mg/kg) or preblocking doses of unlabeled P943 (0.2 mg/kg) and imaged with [11C]P943 PET. Receptor occupancy by the low dose of fenfluramine (1 mg/kg) in the baboons was 25 and 29% and by the high dose of fenfluramine (5 mg/kg) in the rhesus macaque was 42%. Receptor occupancy by P943 (0.2 mg/kg) was 68 and 86% in the baboons. PET imaging of 5‐HT1B r...</description>
            <author>Synapse</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4784133</comments>
            <pubDate>Sun, 10 Apr 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4784133</guid>        </item>
        <item>
            <title>The metabotropic glutamate receptor antagonist 2‐methyl‐6‐(phenylethynyl) pyridine decreases striatal VGlut2 expression in association with an attenuation of L‐dopa‐induced dyskinesias</title>
            <link>http://www.medworm.com/index.php?rid=4784132&amp;cid=s_33785_25_f&amp;fid=33785&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fsyn.20941</link>
            <description>AbstractThe striatal glutamatergic hyperactivity is considered critical in the development of levodopa‐induced dyskinesias (LID) in Parkinson's disease (PD). Pharmacological antagonism of the metabotropic glutamate receptors (mGluRs), in particular, the subtype mGluR5, can inhibit the expression of dyskinesia in both rodent and nonhuman primate models of PD. However, the exact mechanisms underlying the mGluR5 antagonism effects are not completely known. The vesicular glutamate transporters (VGluts) are localized in the synaptic vesicles of the striatal glutamatergic axonal terminals. The effects of mGluR5 antagonism modulating VGlut1 and VGlut2, as selective markers for the corticostriatal and thalamostriatal pathways, respectively, are still unknown. We investigated the effects of the m...</description>
            <author>Synapse</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4784132</comments>
            <pubDate>Sun, 10 Apr 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4784132</guid>        </item>
        <item>
            <title>The metabotropic glutamate receptor antagonist MPEP decreases striatal VGLUT2 expression in association with an attenuation of L‐Dopa induced dyskinesias</title>
            <link>http://www.medworm.com/index.php?rid=4699641&amp;cid=s_33785_25_f&amp;fid=33785&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fsyn.20941</link>
            <description>AbstractThe striatal glutamatergic hyperactivity is considered critical in the development of levodopa‐induced dyskinesias (LID) in Parkinson's disease (PD). Pharmacological antagonism of the metabotropic glutamate receptors (mGluRs), in particular the subtype mGluR5, can inhibit the expression of dyskinesia in both rodent and non‐human primate models of PD. However, the exact mechanisms underlying the mGluR5 antagonism effects are not completely known. The vesicular glutamate transporters (VGluts) are localized in the synaptic vesicles of the striatal glutamatergic axonal terminals. The effects of mGluR5 antagonism modulating VGlut1 and VGlut2, as selective markers for the corticostriatal and thalamostriatal pathways, respectively, are still unknown. We investigated the effects of the...</description>
            <author>Synapse</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4699641</comments>
            <pubDate>Sun, 10 Apr 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4699641</guid>        </item>
        <item>
            <title>Apamin induces plastic changes in hippocampal neurons in senile Sprague‐Dawley rats</title>
            <link>http://www.medworm.com/index.php?rid=4672530&amp;cid=s_33785_25_f&amp;fid=33785&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fsyn.20938</link>
            <description>AbstractApamin is a neurotoxin extracted from honey bee venom and is a selective blocker of small conductance Ca2+ ‐activated K+ channels (SK). Several behavioral and electrophysiological studies indicate that SK‐blockade by apamin may enhance neuron excitability, synaptic plasticity and long‐term potentiation (LTP) in the CA1 hippocampal region, and for that reason, apamin has been proposed as a therapeutic agent in Alzheimer's disease treatment. However, the dendritic morphological mechanisms implied in such enhancement are unknown. In the present work, Golgi‐Cox stain protocol and Sholl analysis were used to study the effect of apamin on the dendritic morphology of pyramidal neurons from hippocampus and the prefrontal cortex, as well as on the medium spiny neurons from the nucle...</description>
            <author>Synapse</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4672530</comments>
            <pubDate>Mon, 04 Apr 2011 20:46:26 +0100</pubDate>
            <guid isPermaLink="false">4672530</guid>        </item>
        <item>
            <title>Lack of association between synapsin II (SYN2) gene polymorphism and susceptibility epilepsy: A case–control study and meta‐analysis</title>
            <link>http://www.medworm.com/index.php?rid=4833523&amp;cid=s_33785_25_f&amp;fid=33785&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fsyn.20939</link>
            <description>Conclusions: Our study indicated that SYN2 rs3773364 A&amp;gt;G polymorphism is not a risk factor for susceptibility to epilepsy. Synapse 2011. © 2011 Wiley‐Liss, Inc. (Source: Synapse)</description>
            <author>Synapse</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4833523</comments>
            <pubDate>Sun, 03 Apr 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4833523</guid>        </item>
        <item>
            <title>Apamin induces plastic changes in hippocampal neurons in senile Sprague–Dawley rats</title>
            <link>http://www.medworm.com/index.php?rid=4784131&amp;cid=s_33785_25_f&amp;fid=33785&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fsyn.20938</link>
            <description>AbstractApamin is a neurotoxin extracted from honey bee venom and is a selective blocker of small‐conductance Ca2+‐activated K+ channels (SK). Several behavioral and electrophysiological studies indicate that SK‐blockade by apamin may enhance neuron excitability, synaptic plasticity, and long‐term potentiation in the CA1 hippocampal region, and, for that reason, apamin has been proposed as a therapeutic agent in Alzheimer's disease treatment. However, the dendritic morphological mechanisms implied in such enhancement are unknown. In the present work, Golgi–Cox stain protocol and Sholl analysis were used to study the effect of apamin on the dendritic morphology of pyramidal neurons from hippocampus and the prefrontal cortex as well as on the medium spiny neurons from the nucleus a...</description>
            <author>Synapse</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4784131</comments>
            <pubDate>Sun, 03 Apr 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4784131</guid>        </item>
        <item>
            <title>Lack of association between synapsin II (SYN2) gene polymorphism and susceptibility epilepsy: A case –control study and meta‐analysis</title>
            <link>http://www.medworm.com/index.php?rid=4672533&amp;cid=s_33785_25_f&amp;fid=33785&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fsyn.20939</link>
            <description>Conclusions:Our study indicated that SYN2 rs3773364 A&amp;gt;G polymorphism is not a risk factor for susceptibility to epilepsy. Synapse, 2011. © 2011 Wiley‐Liss, Inc. (Source: Synapse)</description>
            <author>Synapse</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4672533</comments>
            <pubDate>Sun, 03 Apr 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4672533</guid>        </item>
        <item>
            <title>Activation of extracellular signal‐regulated kinase is critical for the discriminative stimulus effects induced by U‐50,488H</title>
            <link>http://www.medworm.com/index.php?rid=4672532&amp;cid=s_33785_25_f&amp;fid=33785&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fsyn.20937</link>
            <description>AbstractWe previously demonstrated that the discriminative stimulus effects of the kappa‐opioid receptor agonist U‐50,488H were associated with its aversive effects in rats. However, its molecular signaling mechanisms are not fully understood. The aim of the present study was to investigate the intracellular signaling that plays a role in mediating the discriminative stimulus effect induced by U‐50,488H. To better understand the involvement of molecular signaling mechanisms in the discriminative stimulus effects of U‐50,488H, rats were subjected to a drug discrimination paradigm, and levels of immunoreactivity and mRNA expression were determined in these rats. Although U‐50,488H‐trained rats did not show changes in the mRNA expression of typical dopamine receptors, NMDA recepto...</description>
            <author>Synapse</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4672532</comments>
            <pubDate>Sun, 03 Apr 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4672532</guid>        </item>
        <item>
            <title>COMT Val158Met genotype and striatal D2/3 receptor binding in adults with 22q11 deletion syndrome</title>
            <link>http://www.medworm.com/index.php?rid=4672531&amp;cid=s_33785_25_f&amp;fid=33785&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fsyn.20932</link>
            <description>AbstractAlthough catechol‐O‐methyltransferase (COMT) activity evidently affects dopamine function in prefrontal cortex, the contribution in striatum is assumed less significant. We studied whether a functional polymorphism in the COMT gene (Val158Met) influences striatal D2/3R binding ratios (D2/3R BPND) in fifteen adults with 22q11 deletion syndrome and hemizygous for this gene, using single photon emission computed tomography (SPECT) and the selective D2/3 radioligand [123I]IBZM. Met hemizygotes had significantly lower mean D2/3R BPND than Val hemizygotes. These preliminary data suggest that low COMT activity may affect dopamine levels in striatum in humans and this may have implications for understanding the contribution of COMT activity to psychiatric disorders. Synapse, 2011. © 2...</description>
            <author>Synapse</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4672531</comments>
            <pubDate>Sun, 03 Apr 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4672531</guid>        </item>
        <item>
            <title>Cocaine increases ryanodine receptors via dopamine D1 receptors</title>
            <link>http://www.medworm.com/index.php?rid=4646211&amp;cid=s_33785_25_f&amp;fid=33785&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fsyn.20935</link>
            <description>This study attempted to investigate regulatory mechanisms of RyR expression using the cerebral cortical neurons in primary culture intermittently exposed to a psychostimulant, cocaine. Intermittent exposure to cocaine (10 μM) significantly enhanced RyR 1 and 2 proteins and their mRNA, but not RyR 3 expression in the neurons. These cocaine‐induced increases of RyR proteins and their mRNA were dose‐dependently blocked by a dopamine D1 receptor antagonist (SCH23390), but not by a dopamine D2 receptor antagonist (sulpiride). These results indicate a regulatory role of dopamine D1 receptors in RyR expression by cocaine. Synapse, 2011. © 2011 Wiley‐Liss, Inc. (Source: Synapse)</description>
            <author>Synapse</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4646211</comments>
            <pubDate>Tue, 29 Mar 2011 18:27:09 +0100</pubDate>
            <guid isPermaLink="false">4646211</guid>        </item>
        <item>
            <title>In vivo effects of pardoprunox (SLV308), a partial D2/D3 receptor and 5‐HT1A receptor agonist, on rat dopamine and serotonin neuronal activity</title>
            <link>http://www.medworm.com/index.php?rid=4646212&amp;cid=s_33785_25_f&amp;fid=33785&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fsyn.20936</link>
            <description>AbstractThe non‐ergot ligand pardoprunox (SLV308) is a dopamine (DA) D2/D3 and serotonin (5‐HT)1A receptor agonist and a new candidate for the treatment of Parkinson's disease. We used in vivo electrophysiological paradigms in the rat to assess the effects of pardoprunox on DA neuronal activity in ventral tegmental area (VTA) and substantia nigra pars compacta (SNc) as well as on 5‐HT neuronal activity in dorsal raphe nucleus (DRN). In the VTA, pardoprunox (2‐20 µg/kg, i.v.) decreased partially the firing activity of DA neurons. Interestingly, the bursting activity of VTA DA neurons was completely suppressed. This compound both reversed and prevented the inhibition of firing rate induced by the full D2‐like receptor agonist apomorphine, confirming its partial D2‐like receptor ...</description>
            <author>Synapse</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4646212</comments>
            <pubDate>Sun, 27 Mar 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4646212</guid>        </item>
        <item>
            <title>Lactational and postnatal exposure to PCBs induces sex‐specific anxiolytic behavior and cognitive deficit in mice offspring</title>
            <link>http://www.medworm.com/index.php?rid=4623796&amp;cid=s_33785_25_f&amp;fid=33785&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fsyn.20934</link>
            <description>AbstractThe central nervous system (CNS) is affected by polychlorinated biphenyls (PCBs). Previous studies have indicated that developmental exposure to PCBs impairs behavioral performance and alters cognitive abilities. The current study assessed the effects of lactational and postnatal exposure to a commercial PCBs mixture, Aroclor 1254 (A1254), on mice performing several neurobehavioral tasks including the open field test, novel object test, elevated plus maze (EPM) test, Y‐maze test, and tail suspension test (TST). In the open field test, PCBs treatment (6 and 18 mg/kg/day) was associated with increased movement, time duration, and frequency in the central zone in female but not male mice. PCBs‐treated female mice (6 and 18 mg/kg/day) also showed decreased novel object recognition,...</description>
            <author>Synapse</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4623796</comments>
            <pubDate>Wed, 23 Mar 2011 18:58:04 +0100</pubDate>
            <guid isPermaLink="false">4623796</guid>        </item>
        <item>
            <title>The contribution of low‐affinity transport mechanisms to serotonin clearance in synaptosomes</title>
            <link>http://www.medworm.com/index.php?rid=4688169&amp;cid=s_33785_25_f&amp;fid=33785&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fsyn.20929</link>
            <description>AbstractAlthough many studies assert that the serotonin (5‐HT) transporter (SERT) is the predominant mechanism controlling extracellular 5‐HT concentrations, accumulating evidence suggests that low affinity, high capacity transport mechanisms may contribute more to 5‐HT clearance than previously thought. The goal of this study was to quantify the contributions of SERT relative to other mechanisms in clearing extracellular 5‐HT concentrations ranging from 50 nM to 1 μM in synaptosomes prepared from wild‐type and SERT knockout mice using rotating disk electrode voltammetry. SERT inhibitors combined with decynium‐22 (D‐22), a blocker of several low‐affinity transporters, blocked all uptake of 5‐HT into synaptosomes. We found that SERT is responsible for the majority of syna...</description>
            <author>Synapse</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4688169</comments>
            <pubDate>Mon, 21 Mar 2011 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4688169</guid>        </item>
        <item>
            <title>Lactational and postnatal exposure to polychlorinated biphenyls induces sex‐specific anxiolytic behavior and cognitive deficit in mice offspring</title>
            <link>http://www.medworm.com/index.php?rid=4688168&amp;cid=s_33785_25_f&amp;fid=33785&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fsyn.20934</link>
            <description>This study assessed the effects of lactational and postnatal exposure to a commercial PCBs mixture, Aroclor 1254 (A1254), on mice performing several neurobehavioral tasks including the open field test, novel object test, elevated plus maze test, Y‐maze test, and tail suspension test. In the open field test, PCBs treatment (6 and 18 mg/kg/day) was associated with increased movement, time duration, and frequency in the central zone in female but not male mice. PCBs‐treated female mice (6 and 18 mg/kg/day) also showed decreased novel object recognition, indicating impairment in recognition memory. Finally, we performed autoradiographic receptor binding assays for dopamine (DA) D1 and D2 receptors, dopamine transporter (DAT), and the N‐methyl‐D‐aspartic acid (NMDA) receptor after beh...</description>
            <author>Synapse</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4688168</comments>
            <pubDate>Mon, 21 Mar 2011 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4688168</guid>        </item>
        <item>
            <title>The contribution of low affinity transport mechanisms to serotonin clearance in synaptosomes</title>
            <link>http://www.medworm.com/index.php?rid=4623800&amp;cid=s_33785_25_f&amp;fid=33785&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fsyn.20929</link>
            <description>AbstractAlthough many studies assert that the serotonin (5‐HT) transporter (SERT) is the predominant mechanism controlling extracellular 5‐HT concentrations, accumulating evidence suggests that low affinity, high capacity transport mechanisms may contribute more to 5‐HT clearance than previously thought. The goal of this study was to quantify the contributions of SERT relative to other mechanisms in clearing extracellular 5‐HT concentrations ranging from 50 nM to 1 μM in synaptosomes prepared from wild‐type and SERT knockout mice using rotating disk electrode voltammetry. SERT inhibitors combined with decynium‐22 (D‐22), a blocker of several low affinity transporters, blocked all uptake of 5‐HT into synaptosomes. We found that SERT is responsible for the majority of synapt...</description>
            <author>Synapse</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4623800</comments>
            <pubDate>Mon, 21 Mar 2011 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4623800</guid>        </item>
        <item>
            <title>Possible involvement of β‐endorphin in a loss of the coordinated balance of μ‐opioid receptors trafficking processes by fentanyl</title>
            <link>http://www.medworm.com/index.php?rid=4623799&amp;cid=s_33785_25_f&amp;fid=33785&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fsyn.20930</link>
            <description>AbstractIn the present study, we found that cells expressing μ‐opioid receptors (MOR) that were treated with fentanyl or oxycodone showed robust endocytosis of MOR, while cells treated with morphine showed little endocytosis of MOR. The MOR were recovered to the plasma membrane at 90 min after the washing‐out. However, the internalized MOR induced by fentanyl remained in the cytosolic fraction at 6 hr in the presence of β‐endorphin, whereas the internalized MOR induced by oxycodone with β‐endorphin was time‐dependently recycled to the plasma membrane. The present findings indicate that β‐endorphin prolonged the fentanyl‐induced internalization of MOR in cultured cells. Synapse, 2011. © 2011 Wiley‐Liss, Inc. (Source: Synapse)</description>
            <author>Synapse</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4623799</comments>
            <pubDate>Mon, 21 Mar 2011 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4623799</guid>        </item>
        <item>
            <title>Effects of food restriction and sucrose intake on synaptic delivery of AMPA receptors in nucleus accumbens</title>
            <link>http://www.medworm.com/index.php?rid=4623798&amp;cid=s_33785_25_f&amp;fid=33785&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fsyn.20931</link>
            <description>AbstractInsertion and removal of AMPA receptors from the synaptic membrane underlie dynamic tuning of synaptic transmission and enduring changes in synaptic strength. Preclinical addiction research suggests that AMPA receptor trafficking plays an important role in nucleus accumbens (NAc) neuroplasticity underlying the compulsive and persistent quality of drug‐seeking. Considering the parallels between drug addiction and compulsive eating, plus the supranormal reward properties of sucrose, and the role of dieting as a risk factor in development of binge pathology, the present study used a biochemical subcellular fractionation approach to determine whether brief intake of a 10% sucrose solution increases synaptic delivery of AMPA receptors in NAc of chronically food‐restricted (FR) relat...</description>
            <author>Synapse</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4623798</comments>
            <pubDate>Mon, 21 Mar 2011 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4623798</guid>        </item>
        <item>
            <title>Age‐related changes in gene expression are accelerated in Alzheimer's disease</title>
            <link>http://www.medworm.com/index.php?rid=4623797&amp;cid=s_33785_25_f&amp;fid=33785&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fsyn.20933</link>
            <description>AbstractIn the normal brain, age is associated with changes in gene expression. Age is also a prominent risk factor for Alzheimer's disease (AD), where clinical features are similar to age‐related decreases in cognitive performance. We hypothesized that some age‐related changes in gene expression are accelerated in AD patients. To study this, we selected 10 candidate genes earlier shown by microarray analysis to be differentially expressed in AD (Emilsson et al., 2006). Using real‐time PCR analysis and a control based statistical model we investigated age‐related changes in mRNA levels in a large collection of human brain post‐mortem tissues from AD patients and controls. Our results demonstrate that the age‐related changes in gene expression are manifested earlier in AD. Furth...</description>
            <author>Synapse</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4623797</comments>
            <pubDate>Mon, 21 Mar 2011 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4623797</guid>        </item>
        <item>
            <title>Down‐regulation of gephyrin in temporal lobe epilepsy neurons in humans and a rat model</title>
            <link>http://www.medworm.com/index.php?rid=4583234&amp;cid=s_33785_25_f&amp;fid=33785&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fsyn.20928</link>
            <description>AbstractGephyrin, which is a postsynaptic scaffolding protein participated in clustering GABAA receptors at inhibitory synapses, has been reported to be involved in temporal lobe epilepsy (TLE) recently. Here, we investigate gephyrin protein expression in the temporal lobe epileptic foci in epileptic patients and experimental animals in order to explore the probable relationship between gephyrin expression and TLE. Using immunohistochemistry, immunofluorescence, and western blot analysis, gephyrin expression was examined in thirty human temporal neocortex samples from patients who underwent surgery to treat drug‐refractory TLE and ten histological normal temporal neocortex from the controls. Meanwhile, we investigated the gephyrin expression in the hippocampus and adjacent neocortex from...</description>
            <author>Synapse</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4583234</comments>
            <pubDate>Tue, 15 Mar 2011 15:55:38 +0100</pubDate>
            <guid isPermaLink="false">4583234</guid>        </item>
        <item>
            <title>Downregulation of gephyrin in temporal lobe epilepsy neurons in humans and a rat model</title>
            <link>http://www.medworm.com/index.php?rid=4688167&amp;cid=s_33785_25_f&amp;fid=33785&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fsyn.20928</link>
            <description>AbstractGephyrin, which is a postsynaptic scaffolding protein participated in clustering GABAA receptors at inhibitory synapses, has been reported to be involved in temporal lobe epilepsy (TLE) recently. Here, we investigate gephyrin protein expression in the temporal lobe epileptic foci in epileptic patients and experimental animals in order to explore the probable relationship between gephyrin expression and TLE. Using immunohistochemistry, immunofluorescence, and western blot analysis, gephyrin expression was examined in 30 human temporal neocortex samples from patients who underwent surgery to treat drug‐refractory TLE and 10 histological normal temporal neocortex from the controls. Meanwhile, we investigated the gephyrin expression in the hippocampus and adjacent neocortex from expe...</description>
            <author>Synapse</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4688167</comments>
            <pubDate>Mon, 14 Mar 2011 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4688167</guid>        </item>
        <item>
            <title>Relationship between SLC6A3 genotype and striatal dopamine transporter availability: A meta‐analysis of human single photon emission computed tomography studies</title>
            <link>http://www.medworm.com/index.php?rid=4646216&amp;cid=s_33785_25_f&amp;fid=33785&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fsyn.20927</link>
            <description>AbstractThe human dopamine transporter (DAT) gene (SLC6A3) contains a 40‐bp variable number of tandem repeats (VNTR) polymorphism. A number of studies have investigated the association of this VNTR with striatal DAT availability in humans using single photon emission computed tomography (SPECT). However, the results are not consistent. Therefore, we carried out a meta‐analysis of the association between the SLC6A3 VNTR and striatal DAT binding measured in human SPECT studies. The meta‐analysis of five samples of healthy individuals failed to find a significant difference in DAT availability between SLC6A3 9‐repeat carriers and 10‐repeat homozygotes (P = 0.22) although the 9R carriers had nominally higher striatal DAT levels (g = 0.66). The results remained nonsignificant after th...</description>
            <author>Synapse</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4646216</comments>
            <pubDate>Mon, 14 Mar 2011 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4646216</guid>        </item>
        <item>
            <title>Relationship between SLC6A3 genotype and striatal dopamine transporter availability: A meta‐analysis of human SPECT studies</title>
            <link>http://www.medworm.com/index.php?rid=4583235&amp;cid=s_33785_25_f&amp;fid=33785&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fsyn.20927</link>
            <description>AbstractThe human dopamine transporter (DAT) gene (SLC6A3) contains a 40‐bp variable number of tandem repeats (VNTR) polymorphism. A number of studies have investigated the association of this VNTR with striatal DAT availability in humans using single photon emission computed tomography (SPECT). However, the results are not consistent. Therefore, we carried out a meta‐analysis of the association between the SLC6A3 VNTR and striatal DAT binding measured in human SPECT studies. The meta‐analysis of 5 samples of healthy individuals failed to find a significant difference in DAT availability between SLC6A3 9‐repeat carriers and 10‐repeat homozygotes (p = 0.22) although the 9R carriers had nominally higher striatal DAT levels (g = 0.66). The results remained non‐significant after th...</description>
            <author>Synapse</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4583235</comments>
            <pubDate>Mon, 14 Mar 2011 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4583235</guid>        </item>
        <item>
            <title>Hippocampal mossy fiber LTD in Grm2/3 double knockout mice</title>
            <link>http://www.medworm.com/index.php?rid=4523171&amp;cid=s_33785_25_f&amp;fid=33785&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fsyn.20923</link>
            <description>AbstractGroup II metabotropic glutamate receptors (mGluR2, encoded by Grm2, and mGluR3, encoded by Grm3) are inhibitory autoreceptors that negatively modulate the adenylate cyclase signaling cascade. Within the hippocampus, mGluR2 is believed to play a key role in the induction of long‐term depression (LTD) at mossy fiber‐CA3 synapses. Here we used Grm2/3 double knockout (dko) mice to investigate to what extent group II mGluRs are necessary for mossy fiber LTD. Surprisingly, we found that these mice displayed prominent mossy fiber LTD. However, the induction of this form of LTD was sensitive to the external Ca2+ concentration. Mossy fiber LTD in Grm2/3 dko mice was indistinguishable from that in wild‐type mice at 4 mM Ca2+, but largely absent at 2 mM external Ca2+. Mossy fiber LTD in...</description>
            <author>Synapse</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4523171</comments>
            <pubDate>Sat, 26 Feb 2011 18:35:33 +0100</pubDate>
            <guid isPermaLink="false">4523171</guid>        </item>
        <item>
            <title>Evaluation of dopamine D2/3specific binding in the cerebellum for the positron emission tomography radiotracer [11C]FLB 457: Implications for measuring cortical dopamine release</title>
            <link>http://www.medworm.com/index.php?rid=4755643&amp;cid=s_33785_25_f&amp;fid=33785&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fsyn.20926</link>
            <description>AbstractIn a recent positron emission tomography (PET) study, we demonstrated the ability to measure amphetamine‐induced dopamine (DA) release in the human cortex with the DA D2/3 radioligand [11C]FLB 457. As previous studies in animals have shown that a relatively high fraction of the [11C]FLB 457 signal in the cerebellum represents specific binding to D2/3 receptors, there was concern that the use of the cerebellum as a measure of nonspecific binding (i.e., reference region) to derive [11C]FLB 457 binding potential (BP) (BPND) would bias cortical DA release measurements. Thus, we evaluated the fractional contribution of specific binding to D2/3 receptors in the human cerebellum for [11C]FLB 457. Six healthy human subjects (5M/1F) were studied twice with [11C]FLB 457, once at baseline a...</description>
            <author>Synapse</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4755643</comments>
            <pubDate>Fri, 25 Feb 2011 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4755643</guid>        </item>
        <item>
            <title>D‐cycloserine facilitates extinction of cocaine self‐administration in rats</title>
            <link>http://www.medworm.com/index.php?rid=4646218&amp;cid=s_33785_25_f&amp;fid=33785&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fsyn.20922</link>
            <description>AbstractPrevious research has indicated that D‐cycloserine [DCS; a N‐methyl‐D‐aspartate (NMDA) partial agonist] facilitates the extinction of conditioned fear as well as the extinction of cocaine conditioned place preference. Sprague Dawley rats were first trained to self‐administer cocaine and then we compared their extinction behavior (lever pressing) following treatment with vehicle; 15 mg/kg DCS; or 30 mg/kg DCS. We showed that 30 mg/kg DCS, but not 15 mg/kg significantly accelerated extinction of cocaine self‐administration behavior when compared with saline by almost half (4 days vs. 9 days). At 2 weeks when all animals had extinguished, there were no longer differences between the groups. The present findings support of the potential of NMDA partial agonists as prospecti...</description>
            <author>Synapse</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4646218</comments>
            <pubDate>Fri, 25 Feb 2011 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4646218</guid>        </item>
        <item>
            <title>Inhibition of 3,4‐methylenedioxymethamphetamine metabolism leads to marked decrease in 3,4‐dihydroxymethamphetamine formation but no change in serotonin neurotoxicity: Implications for mechanisms of neurotoxicity</title>
            <link>http://www.medworm.com/index.php?rid=4646215&amp;cid=s_33785_25_f&amp;fid=33785&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fsyn.20925</link>
            <description>Abstract3,4‐Methylenedioxymethamphetamine (MDMA)'s O‐demethylenated metabolite, 3,4‐dihydroxymethamphetamine (HHMA), has been hypothesized to serve as a precursor for the formation of toxic catechol‐thioether metabolites (e.g., 5‐N‐acetylcystein‐S‐yl‐HHMA) that mediate MDMA neurotoxicity. To further test this hypothesis, HHMA formation was blocked with dextromethorphan (DXM), which competitively inhibits cytochrome P450 enzyme‐mediated O‐demethylenation of MDMA to HHMA. In particular, rats were randomly assigned to one of four treatment groups (n = 9–12 per group): (1) Saline/MDMA; (2) DXM/MDMA; (3) DXM/Saline; (4) Saline/Saline. During drug exposure, time‐concentration profiles of MDMA and its metabolites were determined, along with body temperature. One week lat...</description>
            <author>Synapse</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4646215</comments>
            <pubDate>Fri, 25 Feb 2011 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4646215</guid>        </item>
        <item>
            <title>Hippocampal mossy fiber long‐term depression in Grm2/3 double knockout mice</title>
            <link>http://www.medworm.com/index.php?rid=4646214&amp;cid=s_33785_25_f&amp;fid=33785&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fsyn.20923</link>
            <description>AbstractGroup II metabotropic glutamate receptors (mGluR2, encoded by Grm2, and mGluR3, encoded by Grm3) are inhibitory autoreceptors that negatively modulate the adenylate cyclase signaling cascade. Within the hippocampus, mGluR2 is believed to play a key role in the induction of long‐term depression (LTD) at mossy fiber‐CA3 synapses. Here, we used Grm2/3 double knockout (dko) mice to investigate to what extent group II mGluRs are necessary for mossy fiber LTD. Surprisingly, we found that these mice displayed prominent mossy fiber LTD. However, the induction of this form of LTD was sensitive to the external Ca2+ concentration. Mossy fiber LTD in Grm2/3 dko mice was indistinguishable from that in wild‐type mice at 4 mM Ca2+, but largely absent at 2 mM external Ca2+. Mossy fiber LTD i...</description>
            <author>Synapse</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4646214</comments>
            <pubDate>Fri, 25 Feb 2011 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4646214</guid>        </item>
        <item>
            <title>Evaluation of dopamine D2/3 specific binding in the cerebellum for the PET radiotracer [11C]FLB 457: Implications for measuring cortical dopamine release</title>
            <link>http://www.medworm.com/index.php?rid=4523175&amp;cid=s_33785_25_f&amp;fid=33785&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fsyn.20926</link>
            <description>AbstractIn a recent PET study we demonstrated the ability to measure amphetamine‐induced DA release in the human cortex with the dopamine D2/3 radioligand [11C]FLB 457. As previous studies in animals have shown that a relatively high fraction of the [11C]FLB 457 signal in the cerebellum represents specific binding to D2/3 receptors, there was concern that the use of the cerebellum as a measure of nonspecific binding (i.e., reference region) to derive [11C]FLB 457 binding potential (BPND) would bias cortical dopamine release measurements. Thus, we evaluated the fractional contribution of specific binding to D2/3 receptors in the human cerebellum for [11C]FLB 457.Six healthy human subjects (5M/1F) were studied twice with [11C]FLB 457, once at baseline and again following a single oral dose...</description>
            <author>Synapse</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4523175</comments>
            <pubDate>Fri, 25 Feb 2011 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4523175</guid>        </item>
        <item>
            <title>Altered expression of Dscam in temporal lobe tissue from human and experimental animals</title>
            <link>http://www.medworm.com/index.php?rid=4523174&amp;cid=s_33785_25_f&amp;fid=33785&amp;url=http%3A%2F%2Fdx.doi.org%2F10.1002%252Fsyn.20924</link>
            <description>AbstractDown syndrome cell adhesion molecule (Dscam) is a neural adhesion molecule that plays an essential role in the establishment of neural circuits. Considerable evidence suggests that Dscam is required for axon guidance and dendritic arborization. Our aim was to investigate the expression of Dscam in the temporal lobes of patients with intractable epilepsy (IE) and of experimental animals. In the present study, we used immunohistochemistry immunofluorescence and western blotting to examine Dscam expression in thirty‐five surgical samples from brains of IE patients and 15 control brain samples. We also measured the levels of Dscam during the entire epileptic process in a rat model of temporal lobe epilepsy. Dscam expression in IE patients was significantly higher compared to that in ...</description>
            <author>Synapse</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4523174</comments>
            <pubDate>Fri, 25 Feb 2011 00:00:00 +0100</pubDate>
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