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        <title>Molecular Brain 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 'Molecular Brain' source.</description>
        <link><![CDATA[http://www.medworm.com/rss/search.php?qu=Molecular+Brain&t=Molecular+Brain&s=Search&f=source]]></link>
        <lastBuildDate>Sun, 14 Mar 2010 16:32:18 +0100</lastBuildDate>
        <item>
            <title>Depression research: where are we now?</title>
            <link>http://www.medworm.com/index.php?rid=3350117&amp;cid=s_37189_168_f&amp;fid=37189&amp;url=http%3A%2F%2Fwww.molecularbrain.com%2Fcontent%2F3%2F1%2F8</link>
            <description>Extensive studies have led to a variety of hypotheses for the molecular basis of depression and related mood disorders, but a definite pathogenic mechanism has yet to be defined. The monoamine hypothesis, in conjunction with the efficacy of antidepressants targeting monoamine systems, has long been the central topic of depression research. While it is widely embraced that the initiation of antidepressant efficacy may involve acute changes in monoamine systems, apparently, the focus of current research is moving toward molecular mechanisms that underlie long-lasting downstream changes in the brain after chronic antidepressant treatment, thereby reaching for a detailed view of the pathophysiology of depression and related mood disorders. In this minireview, we briefly summarize major themes ...</description>
            <author>Molecular Brain</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3350117</comments>
            <pubDate>Wed, 10 Mar 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3350117</guid>        </item>
        <item>
            <title>Scanning mutagenesis of the I-II loop of the Cav2.2 calcium channel identifies residues Arginine 376 and Valine 416 as molecular determinants of voltage dependent G protein inhibition</title>
            <link>http://www.medworm.com/index.php?rid=3314519&amp;cid=s_37189_168_f&amp;fid=37189&amp;url=http%3A%2F%2Fwww.molecularbrain.com%2Fcontent%2F3%2F1%2F6</link>
            <description>Direct interaction with the β subunit of the heterotrimeric G protein complex causes voltage-dependent inhibition of N-type calcium channels. To further characterize the molecular determinants of this interaction, we performed scanning mutagenesis of residues 372-387 and 410-428 of the N-type channel α1 subunit, in which individual residues were replaced by either alanine or cysteine. We coexpressed wild type Gβ1γ2 subunits with either wild type or point mutant N-type calcium channels, and voltage-dependent, G protein-mediated inhibition of the channels (VDI) was assessed using patch clamp recordings. The resulting data indicate that Arg376 and Val416 of the α1 subunit, residues which are surface-exposed in the presence of the calcium channel β subunit, contribute significantly to th...</description>
            <author>Molecular Brain</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3314519</comments>
            <pubDate>Wed, 03 Feb 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3314519</guid>        </item>
        <item>
            <title>Scanning mutagenesis of the I-II loop of the Cav2.2 calcium channel identifies residues Arginine 376 and Valine 416 as molecular determinants of voltage dependent G protein inhibition</title>
            <link>http://www.medworm.com/index.php?rid=3294460&amp;cid=s_37189_168_f&amp;fid=37189&amp;url=http%3A%2F%2Fwww.molecularbrain.com</link>
            <description>Direct interaction with the beta subunit of the heterotrimeric G protein complex causes voltage-dependent inhibition of N-type calcium channels. To further characterize the molecular determinants of this interaction, we performed scanning mutagenesis of residues 372-387 and 410-428 of the N-type channel alpha1 subunit, in which individual residues were replaced by either alanine or cysteine. We coexpressed wild type G beta1 gamma2 subunits with either wild type or point mutant N-type calcium channels, and voltage-dependent, G protein-mediated inhibition of the channels (VDI) was assessed using patch clamp recordings. The resulting data indicate that Arg376 and Val416 of the alpha1 subunit, residues which are surface-exposed in the presence of the calcium channel beta subunit, contribute si...</description>
            <author>Molecular Brain</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3294460</comments>
            <pubDate>Wed, 03 Feb 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3294460</guid>        </item>
        <item>
            <title>Scanning mutagenesis of the I-II loop of the Cav2.2 calcium channel identifies residues Arginine 377 and Valine 416 as molecular determinants of voltage dependent G protein inhibition</title>
            <link>http://www.medworm.com/index.php?rid=3239317&amp;cid=s_37189_168_f&amp;fid=37189&amp;url=http%3A%2F%2Fwww.molecularbrain.com%2Fcontent%2F3%2F1%2F6</link>
            <description>Direct interaction with the beta subunit of the heterotrimeric G protein complex causes voltage-dependent inhibition of N-type calcium channels. To further characterize the molecular determinants of this interaction, we performed scanning mutagenesis of residues 372-387 and 410-428 of the N-type channel alpha1 subunit, in which individual residues were replaced by either alanine or cysteine. We coexpressed wild type G beta1 gamma2 subunits with either wild type or point mutant N-type calcium channels, and voltage-dependent, G protein-mediated inhibition of the channels (VDI) was assessed using patch clamp recordings. The resulting data indicate that Arg376 and Val416 of the alpha1 subunit, residues which are surface-exposed in the presence of the calcium channel beta subunit, contribute si...</description>
            <author>Molecular Brain</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3239317</comments>
            <pubDate>Wed, 03 Feb 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3239317</guid>        </item>
        <item>
            <title>&quot;Color Timer&quot; mice: visualization of neuronal differentiation with fluorescent proteins</title>
            <link>http://www.medworm.com/index.php?rid=3231245&amp;cid=s_37189_168_f&amp;fid=37189&amp;url=http%3A%2F%2Fwww.molecularbrain.com%2Fcontent%2F3%2F1%2F5</link>
            <description>In this study we report the initial version of such a mouse system, which we call &quot;Color Timer.&quot; We first generated transgenic (Tg; nestin/KOr Tg) mice in which production of the fluorescent protein Kusabira-Orange (KOr) is controlled by the gene regulatory elements within the 2nd intronic enhancer of the nestin gene, which is a good marker for NSCs, so that NSCs would emit orange fluorescence upon excitation. We then confirmed by immunohistochemical and immunocytochemical analyses that the KOr fluorescence closely reflected the presence of the Nestin protein. We also confirmed by a neurosphere formation assay that the intensity of the KOr fluorescence correlated with &quot;stemness&quot; and it was possible to readily identify NSCs in the two neurogenic regions, namely the dentate gyrus of the hipp...</description>
            <author>Molecular Brain</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3231245</comments>
            <pubDate>Tue, 02 Feb 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3231245</guid>        </item>
        <item>
            <title>DREAM (Downstream Regulatory Element Antagonist Modulator) contributes to synaptic depression and contextual fear memory</title>
            <link>http://www.medworm.com/index.php?rid=3193585&amp;cid=s_37189_168_f&amp;fid=37189&amp;url=http%3A%2F%2Fwww.molecularbrain.com%2Fcontent%2F3%2F1%2F3</link>
            <description>The downstream regulatory element antagonist modulator (DREAM), a multifunctional Ca2+-binding protein, binds specifically to DNA and several nucleoproteins regulating gene expression and with proteins outside the nucleus to regulate membrane excitability or calcium homeostasis. DREAM is highly expressed in the central nervous system including the hippocampus and cortex; however, the roles of DREAM in hippocampal synaptic transmission and plasticity have not been investigated. Taking advantage of transgenic mice overexpressing a Ca2+-insensitive DREAM mutant (TgDREAM), integrative methods including electrophysiology, biochemistry, immunostaining, and behavior tests were used to study the function of DREAM in synaptic transmission, long-term plasticity and fear memory in hippocampal CA1 reg...</description>
            <author>Molecular Brain</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3193585</comments>
            <pubDate>Thu, 21 Jan 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3193585</guid>        </item>
        <item>
            <title>Pyk2 uncouples metabotropic glutamate receptor G protein signaling but facilitates ERK1/2 activation</title>
            <link>http://www.medworm.com/index.php?rid=3193584&amp;cid=s_37189_168_f&amp;fid=37189&amp;url=http%3A%2F%2Fwww.molecularbrain.com%2Fcontent%2F3%2F1%2F4</link>
            <description>Group I metabotropic glutamate receptors (mGluRs) are coupled via Galphaq/11 to the activation of phospholipase C beta, which hydrolyzes membrane phospholipids to form inositol 1,4,5 trisphosphate and diacylglycerol. This results in the release of Ca2+ from intracellular stores and the activation of protein kinase C. The activation of Group I mGluRs also results in ERK1/2 phosphorylation. We show here, that the proline-rich tyrosine kinase 2 (Pyk2) interacts with both mGluR1 and mGluR5 and is precipitated with both receptors from rat brain. Pyk2 also interacts with GST-fusion proteins corresponding to the second intracellular loop and the distal carboxyl-terminal tail domains of mGluR1a. Pyk2 colocalizes with mGluR1a at the plasma membrane in human embryonic kidney (HEK293) cells and with ...</description>
            <author>Molecular Brain</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3193584</comments>
            <pubDate>Thu, 21 Jan 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3193584</guid>        </item>
        <item>
            <title>Corticosteroids: way upstream</title>
            <link>http://www.medworm.com/index.php?rid=3163613&amp;cid=s_37189_168_f&amp;fid=37189&amp;url=http%3A%2F%2Fwww.molecularbrain.com%2Fcontent%2F3%2F1%2F2</link>
            <description>This article will draw on experience and knowledge derived from studies of the neural actions of other steroid hormones, in particular estrogens, not only because there are many parallels but also because 'learning from differences' can be a fruitful approach. The core purpose of this review is to consider the mechanisms through which corticosteroids might act rapidly to alter neural signaling. (Source: Molecular Brain)</description>
            <author>Molecular Brain</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3163613</comments>
            <pubDate>Mon, 11 Jan 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3163613</guid>        </item>
        <item>
            <title>The transcription factor RBP-J is essential for retinal cell differentiation and lamination</title>
            <link>http://www.medworm.com/index.php?rid=3100538&amp;cid=s_37189_168_f&amp;fid=37189&amp;url=http%3A%2F%2Fwww.molecularbrain.com%2Fcontent%2F2%2F1%2F38</link>
            <description>Conclusions:
Our data indicate that RBP-J-mediated canonical Notch signaling governs retinal cell specification and differentiation, and maintains retinal lamination through the expression of b-catenin. (Source: Molecular Brain)</description>
            <author>Molecular Brain</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3100538</comments>
            <pubDate>Fri, 18 Dec 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3100538</guid>        </item>
        <item>
            <title>Action potential evoked transmitter release in central synapses: insights from the developing calyx of Held</title>
            <link>http://www.medworm.com/index.php?rid=3026493&amp;cid=s_37189_168_f&amp;fid=37189&amp;url=http%3A%2F%2Fwww.molecularbrain.com%2Fcontent%2F2%2F1%2F36</link>
            <description>Chemical synapses are the fundamental units that mediate communication between neurons in the mammalian brain. In contrast to the enormous progress made in mapping out postsynaptic contributions of receptors, scaffolding structures and receptor trafficking to synaptic transmission and plasticity, the small size of nerve terminals has largely precluded direct analyses of presynaptic modulation of excitability and transmitter release in central synapses. Recent studies performed in accessible synapses such as the calyx of Held, a giant axosomatic synapse in the sound localization circuit of the auditory brainstem, have provided tremendous insights into how central synapses regulate the dynamic gain range of synaptic transmission. This review will highlight experimental evidence that resolves...</description>
            <author>Molecular Brain</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3026493</comments>
            <pubDate>Wed, 25 Nov 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3026493</guid>        </item>
        <item>
            <title>Abnormalities in brain structure and behavior in GSK-3 mutant mice</title>
            <link>http://www.medworm.com/index.php?rid=3012178&amp;cid=s_37189_168_f&amp;fid=37189&amp;url=http%3A%2F%2Fwww.molecularbrain.com%2Fcontent%2F2%2F1%2F35</link>
            <description>Conclusions:
Taken together, our data support a role for the GSK-3alpha gene in CNS functioning and possible involvement in the development of psychiatric disorders. (Source: Molecular Brain)</description>
            <author>Molecular Brain</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3012178</comments>
            <pubDate>Thu, 19 Nov 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3012178</guid>        </item>
        <item>
            <title>CBP/p300 is a cell type-specific modulator of CLOCK/BMAL1-mediated transcription</title>
            <link>http://www.medworm.com/index.php?rid=3007813&amp;cid=s_37189_168_f&amp;fid=37189&amp;url=http%3A%2F%2Fwww.molecularbrain.com%2Fcontent%2F2%2F1%2F34</link>
            <description>Conclusions:
Our findings indicate possible mechanisms by which CBP/p300 tissue-specifically acts cooperatively with pCAF and HDAC3 either as a co-activator or co-repressor, respectively, for CLOCK/BMAL1. (Source: Molecular Brain)</description>
            <author>Molecular Brain</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3007813</comments>
            <pubDate>Thu, 19 Nov 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3007813</guid>        </item>
        <item>
            <title>Genetic and pharmacological inhibition of calcineurin corrects the BDNF transport defect in Huntington's disease</title>
            <link>http://www.medworm.com/index.php?rid=2930821&amp;cid=s_37189_168_f&amp;fid=37189&amp;url=http%3A%2F%2Fwww.molecularbrain.com%2Fcontent%2F2%2F1%2F33</link>
            <description>Huntington's disease (HD) is an inherited neurogenerative disease caused by an abnormal expansion of glutamine repeats in the huntingtin protein. There is currently no treatment to prevent the neurodegeneration caused by this devastating disorder. Huntingtin has been shown to be a positive regulator of vesicular transport, particularly for neurotrophins such as brain-derived neurotrophic factor (BDNF). This function is lost in patients with HD, resulting in a decrease in neurotrophic support and subsequent neuronal death. One promising line of treatment is therefore the restoration of huntingtin function in BDNF transport. (Source: Molecular Brain)</description>
            <author>Molecular Brain</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2930821</comments>
            <pubDate>Tue, 27 Oct 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">2930821</guid>        </item>
        <item>
            <title>Characterization of intracortical synaptic connections in the mouse anterior cingulate cortex using dual patch clamp recording</title>
            <link>http://www.medworm.com/index.php?rid=2894342&amp;cid=s_37189_168_f&amp;fid=37189&amp;url=http%3A%2F%2Fwww.molecularbrain.com%2Fcontent%2F2%2F1%2F32</link>
            <description>The anterior cingulate cortex (ACC) is involved in sensory, cognitive and executive functions. Studies of synaptic transmission and plasticity in the ACC provide basic cellular and molecular mechanisms for brain functions. Previous anatomic studies suggest complex local interactions between neurons within the ACC. However, there is lack of functional studies of such synaptic connections between ACC neurons. In the present study, we characterized the neuronal connections in the superficial layers (I-III) of the mouse ACC using dual whole-cell patch clamp recording technique. Four types of synaptic connections were observed, which are from a pyramidal neuron to a pyramidal neuron, from a pyramidal neuron to an interneuron, from an interneuron to a pyramidal neuron and from an interneuron to ...</description>
            <author>Molecular Brain</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2894342</comments>
            <pubDate>Wed, 14 Oct 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2894342</guid>        </item>
        <item>
            <title>NADPH oxidase mediates beta-amyloid peptide-induced activation of ERK in hippocampal organotypic cultures</title>
            <link>http://www.medworm.com/index.php?rid=2865478&amp;cid=s_37189_168_f&amp;fid=37189&amp;url=http%3A%2F%2Fwww.molecularbrain.com%2Fcontent%2F2%2F1%2F31</link>
            <description>Conclusions: Our findings indicate that NADPH oxidase-dependent redox signaling is required for A-beta-induced activation of ERK, and suggest a similar mechanism may occur during early stages of Alzheimer's disease. (Source: Molecular Brain)</description>
            <author>Molecular Brain</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2865478</comments>
            <pubDate>Sun, 04 Oct 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2865478</guid>        </item>
        <item>
            <title>The emerging role of autophagy in Parkinson's disease</title>
            <link>http://www.medworm.com/index.php?rid=2800183&amp;cid=s_37189_168_f&amp;fid=37189&amp;url=http%3A%2F%2Fwww.molecularbrain.com%2Fcontent%2F2%2F1%2F29</link>
            <description>Parkinson's disease (PD) is the most common neurodegenerative movement disorder that affects about 1% of the population worldwide. Despite significant advances in the identification of genetic mutations and signaling pathways that are associated with the disease, the precise mechanisms implicated in the pathophysiology of the disease are not well understood. More importantly, treatments that are effective in reversing the progression of the disease is essentially lacking. Further investigation into the pathogenic mechanisms of PD thus presents a pressing concern for neuroscientists. Recently, deregulation of the autophagic pathway is observed in the brains of PD patients and in models of PD. In this review we summarize current literature on the emerging involvement of autophagy in PD, and ...</description>
            <author>Molecular Brain</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2800183</comments>
            <pubDate>Tue, 15 Sep 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2800183</guid>        </item>
        <item>
            <title>A riot of rhythms: neuronal and glial circadian oscillators in the mediobasal hypothalamus</title>
            <link>http://www.medworm.com/index.php?rid=2741157&amp;cid=s_37189_168_f&amp;fid=37189&amp;url=http%3A%2F%2Fwww.molecularbrain.com%2Fcontent%2F2%2F1%2F28</link>
            <description>Conclusions:
Our results provide the first single cell resolution of endogenous circadian rhythms in clock gene expression in any intact tissue outside the SCN, reveal the cellular basis for tissue level damping in extra-SCN oscillators and demonstrate that an oscillator in the ME/PT is responsive to changing metabolic environments. (Source: Molecular Brain)</description>
            <author>Molecular Brain</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2741157</comments>
            <pubDate>Wed, 26 Aug 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2741157</guid>        </item>
        <item>
            <title>Multiple functions of precursor BDNF to CNS neurons: negative regulation of neurite growth, spine formation and cell survival</title>
            <link>http://www.medworm.com/index.php?rid=2695125&amp;cid=s_37189_168_f&amp;fid=37189&amp;url=http%3A%2F%2Fwww.molecularbrain.com%2Fcontent%2F2%2F1%2F27</link>
            <description>Conclusions:
These results suggest that proBDNF has distinct functions in different populations of CNS neurons and might be responsible for specific physiological cellular processes in the brain. (Source: Molecular Brain)</description>
            <author>Molecular Brain</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2695125</comments>
            <pubDate>Wed, 12 Aug 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2695125</guid>        </item>
        <item>
            <title>cGMP-dependent protein kinase Ialpha associates with the antidepressant-sensitive serotonin transporter and dictates rapid modulation of serotonin uptake</title>
            <link>http://www.medworm.com/index.php?rid=2733895&amp;cid=s_37189_168_f&amp;fid=37189&amp;url=http%3A%2F%2Fwww.molecularbrain.com%2Fcontent%2F2%2F1%2F26</link>
            <description>Conclusion:
Our findings provide evidence of a physical and compartmentalized association between SERT and PKGIα that supports rapid, 8-Br-cGMP-induced regulation of SERT. We discuss a model wherein SERT-associated PKGIα supports sequentially the mobilization of intracellular transporter-containing vesicles, leading to enhanced surface expression, and the production of catalytic-modulatory SERT phosphorylation, leading to a maximal enhancement of 5-HT clearance capacity. (Source: Molecular Brain)</description>
            <author>Molecular Brain</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2733895</comments>
            <pubDate>Tue, 04 Aug 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2733895</guid>        </item>
        <item>
            <title>cGMP-dependent protein kinase Ialpha associates with the antidepressant-sensitive serotonin transporter and dictates rapid modulation of  serotonin uptake</title>
            <link>http://www.medworm.com/index.php?rid=2674141&amp;cid=s_37189_168_f&amp;fid=37189&amp;url=http%3A%2F%2Fwww.molecularbrain.com%2Fcontent%2F2%2F1%2F26</link>
            <description>Conclusions:
Our findings provide evidence of a physical, and compartmentalized association between SERT and PKGIalpha that supports rapid, 8-Br-cGMP induced regulation of SERT. We discuss a model wherein SERT-associated PKGIalpha supports sequentially the mobilization of intracellular transporter-containing vesicles, leading to enhanced surface expression, and the production of catalytic-modulatory SERT phosphorylation, leading to a maximal enhancement of 5-HT clearance capacity. (Source: Molecular Brain)</description>
            <author>Molecular Brain</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2674141</comments>
            <pubDate>Tue, 04 Aug 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2674141</guid>        </item>
        <item>
            <title>Basic mechanisms for recognition and transport of synaptic cargos</title>
            <link>http://www.medworm.com/index.php?rid=2670676&amp;cid=s_37189_168_f&amp;fid=37189&amp;url=http%3A%2F%2Fwww.molecularbrain.com%2Fcontent%2F2%2F1%2F25</link>
            <description>Synaptic cargo trafficking is essential for synapse formation, function and plasticity. In order to transport synaptic cargo, such as synaptic vesicle precursors, mitochondria, neurotransmitter receptors and signaling proteins to their site of action, neurons make use of molecular motor proteins. These motors operate on the microtubule and actin cytoskeleton and are highly regulated so that different cargos can be transported to distinct synaptic specializations at both pre- and post-synaptic sites. How synaptic cargos achieve specificity, directionality and timing of transport is a developing area of investigation. Recent studies demonstrate that the docking of motors to their cargos is a key control point. Moreover, precise spatial and temporal regulation of motor-cargo interactions is i...</description>
            <author>Molecular Brain</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2670676</comments>
            <pubDate>Mon, 03 Aug 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2670676</guid>        </item>
        <item>
            <title>Autophagy activation and enhanced mitophagy characterize the Purkinje cells of pcdmice prior to neuronal death</title>
            <link>http://www.medworm.com/index.php?rid=2719541&amp;cid=s_37189_168_f&amp;fid=37189&amp;url=http%3A%2F%2Fwww.molecularbrain.com%2Fcontent%2F2%2F1%2F24</link>
            <description>Purkinje cells are a class of specialized neurons in the cerebellum, and are among the most metabolically active of all neurons, as they receive immense synaptic stimulation, and provide the only efferent output from the cerebellum. Degeneration of Purkinje cells is a common feature of inherited ataxias in humans and mice. To understand Purkinje neuron degeneration, investigators have turned to naturally occurring Purkinje cell degeneration phenotypes in mice to identify key regulatory proteins and cellular pathways. The Purkinje cell degeneration (pcd) mouse is a recessive mutant characterized by complete and dramatic post-natal, cell autonomous Purkinje neuron degeneration and death. As the basis of Purkinje cell death in pcd is unresolved, and contradictory data has emerged for the role...</description>
            <author>Molecular Brain</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2719541</comments>
            <pubDate>Tue, 28 Jul 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2719541</guid>        </item>
        <item>
            <title>Autophagy activation and enhanced mitophagy characterize the 
Purkinje cells of pcd mice prior to neuronal death</title>
            <link>http://www.medworm.com/index.php?rid=2653547&amp;cid=s_37189_168_f&amp;fid=37189&amp;url=http%3A%2F%2Fwww.molecularbrain.com%2Fcontent%2F2%2F1%2F24</link>
            <description>Purkinje cells are a class of specialized neurons in the cerebellum, and are among the most metabolically active of all neurons, as they receive immense synaptic stimulation, and provide the only efferent output from the cerebellum. Degeneration of Purkinje cells is a common feature of inherited ataxias in humans and mice. To understand Purkinje neuron degeneration, investigators have turned to naturally occurring Purkinje cell degeneration phenotypes in mice to identify key regulatory proteins and cellular pathways. The Purkinje cell degeneration (pcd) mouse is a recessive mutant characterized by complete and dramatic post-natal, cell autonomous Purkinje neuron degeneration and death. As the basis of Purkinje cell death in pcd is unresolved, and contradictory data has emerged for the role...</description>
            <author>Molecular Brain</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2653547</comments>
            <pubDate>Tue, 28 Jul 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2653547</guid>        </item>
        <item>
            <title>Regulation of endosomal motility and degradation by amyotrophic lateral sclerosis 2/alsin</title>
            <link>http://www.medworm.com/index.php?rid=2637670&amp;cid=s_37189_168_f&amp;fid=37189&amp;url=http%3A%2F%2Fwww.molecularbrain.com%2Fcontent%2F2%2F1%2F23</link>
            <description>Dysfunction of alsin, particularly its putative Rab5 guanine-nucleotide-exchange factor activity, has been linked to one form of juvenile onset recessive familial amyotrophic lateral sclerosis (ALS2). Multiple lines of alsin knockout (ALS2-/-) mice have been generated to model this disease. However, it remains elusive whether the Rab5-dependent endocytosis is altered in ALS2-/- neurons. To directly examine the Rab5-mediated endosomal trafficking in ALS2-/- neurons, we introduced green fluorescent protein-tagged Rab5 into cultured hippocampal neurons to monitor the morphology and motility of Rab5-associated early endosomes. Here we report that Rab5-mediated endocytosis was severely altered in ALS2-/-neurons. Excessive accumulation of Rab5-positive vesicles was observed in ALS2-/- neurons, w...</description>
            <author>Molecular Brain</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2637670</comments>
            <pubDate>Thu, 23 Jul 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2637670</guid>        </item>
        <item>
            <title>A systematic investigation of the protein kinases involved in NMDA receptor-dependent LTD: evidence for a role of GSK-3 but not other serine/threonine kinases</title>
            <link>http://www.medworm.com/index.php?rid=2580051&amp;cid=s_37189_168_f&amp;fid=37189&amp;url=http%3A%2F%2Fwww.molecularbrain.com%2Fcontent%2F2%2F1%2F22</link>
            <description>Conclusions:
The present study is the first to investigate the role of 58 ser/thr protein kinases in LTD in the same study. Of these 58 protein kinases, we have found evidence for the involvement of only one, GSK-3, in LTD. (Source: Molecular Brain)</description>
            <author>Molecular Brain</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2580051</comments>
            <pubDate>Mon, 06 Jul 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2580051</guid>        </item>
        <item>
            <title>Nuclear accumulation of polyglutamine disease proteins and neuropathology</title>
            <link>http://www.medworm.com/index.php?rid=2570032&amp;cid=s_37189_168_f&amp;fid=37189&amp;url=http%3A%2F%2Fwww.molecularbrain.com%2Fcontent%2F2%2F1%2F21</link>
            <description>There are nine inherited neurodegenerative disorders caused by polyglutamine (polyQ) expansion in various disease proteins. Although these polyglutamine proteins have different functions and are localized in different subcellular regions, all the polyQ diseases share a common pathological feature: the nuclear accumulation of polyQ disease proteins and the formation of inclusions. The nuclear accumulation of polyQ proteins in turn leads to gene transcriptional dysregulation and neuropathology. Here we will discuss potential mechanisms behind the nuclear accumulation of mutant polyQ proteins, since an understanding of how polyQ proteins accumulate in the nucleus could help elucidate the pathogenesis of these diseases and develop their treatment. (Source: Molecular Brain)</description>
            <author>Molecular Brain</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2570032</comments>
            <pubDate>Thu, 02 Jul 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2570032</guid>        </item>
        <item>
            <title>Maternal epileptic seizure induced by Pentylenetetrazol: Apoptotic neurodegeneration and decreased GABAB1 receptor expression in prenatal rat brain</title>
            <link>http://www.medworm.com/index.php?rid=2508345&amp;cid=s_37189_168_f&amp;fid=37189&amp;url=http%3A%2F%2Fwww.molecularbrain.com%2Fcontent%2F2%2F1%2F20</link>
            <description>This study for the first time indicate that PTZ-induced seizures triggered activation of caspases-3 to induce widespread apoptotic neuronal death and decreased GABAB1R expression in hippocampal neurons, providing a possible mechanistic link between maternal epilepsy induced neurodegeneration alteration of GABAB1R and PKA expression level during prenatal brain development. This revealed new aspects of PTZ and ethanol's modulation on GABAB1R, learning and memory. Further, explain the possibility that children delivered by epileptic mothers may have higher risk of developmental disturbances and malformations. (Source: Molecular Brain)</description>
            <author>Molecular Brain</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2508345</comments>
            <pubDate>Sun, 21 Jun 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2508345</guid>        </item>
        <item>
            <title>Abnormal social behavior, hyperactivity, impaired remote spatial memory, and increased D1-mediated dopaminergic signaling in neuronal nitric oxide synthase knockout mice</title>
            <link>http://www.medworm.com/index.php?rid=2508346&amp;cid=s_37189_168_f&amp;fid=37189&amp;url=http%3A%2F%2Fwww.molecularbrain.com%2Fcontent%2F2%2F1%2F19</link>
            <description>Conclusions These findings indicate that nNOS KO upregulates dopamine D1 receptor signaling, and induces abnormal social behavior, hyperactivity and impaired remote spatial memory. nNOS KO mice may serve as a unique animal model of psychiatric disorders. (Source: Molecular Brain)</description>
            <author>Molecular Brain</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2508346</comments>
            <pubDate>Wed, 17 Jun 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2508346</guid>        </item>
        <item>
            <title>Hook-up of GluA2, GRIP and liprin-alpha for cholinergic muscarinic receptor-dependent LTD in the hippocampus</title>
            <link>http://www.medworm.com/index.php?rid=2508348&amp;cid=s_37189_168_f&amp;fid=37189&amp;url=http%3A%2F%2Fwww.molecularbrain.com%2Fcontent%2F2%2F1%2F17</link>
            <description>The molecular mechanism underlying muscarinic acetylcholine receptor-dependent LTD (mAChR-LTD) in the hippocampus is less studied. In a recent study, a novel mechanism is described. The induction of mAChR-LTD required the activation of protein tyrosine phosphatase (PTP), and the expression was mediated by AMPA receptor endocytosis via interactions between GluA2, GRIP and liprin-alpha. The hook-up of these proteins may result in the recruitment of leukocyte common antigen-related receptor (LAR), a PTP that is known to be involved in AMPA receptor trafficking. Interestingly, the similar molecular interaction cannot be applied to mGluR-LTD, despite the fact that the same G-protein involved in LTD is activated by both mAChR and mGluR. This discovery provides key molecular insights for choliner...</description>
            <author>Molecular Brain</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2508348</comments>
            <pubDate>Tue, 16 Jun 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2508348</guid>        </item>
        <item>
            <title>A novel mechanism of hippocampal LTD involving muscarinic receptor-triggered interactions between AMPARs, GRIP and liprin-alpha</title>
            <link>http://www.medworm.com/index.php?rid=2508347&amp;cid=s_37189_168_f&amp;fid=37189&amp;url=http%3A%2F%2Fwww.molecularbrain.com%2Fcontent%2F2%2F1%2F18</link>
            <description>Conclusion:
Our results suggest that mAChR-LTD selectively involves interactions between GRIP and liprin-alpha. These data indicate a novel mechanism of synaptic plasticity in which activation of M1 receptors results in AMPAR endocytosis, via a mechanism involving interactions between GluA2, GRIP and liprin-alpha. (Source: Molecular Brain)</description>
            <author>Molecular Brain</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2508347</comments>
            <pubDate>Tue, 16 Jun 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2508347</guid>        </item>
        <item>
            <title>Two major gate-keepers in the self-renewal of neural stem cells: Erk1/2 and PLCgamma1 in FGFR signaling</title>
            <link>http://www.medworm.com/index.php?rid=2463693&amp;cid=s_37189_168_f&amp;fid=37189&amp;url=http%3A%2F%2Fwww.molecularbrain.com%2Fcontent%2F2%2F1%2F15</link>
            <description>Neural stem cells are undifferentiated precursor cells that proliferate, self-renew, and give rise to neuronal and glial lineages. Understanding the molecular mechanisms underlying their self-renewal is an important aspect in neural stem cell biology. The regulation mechanisms governing self-renewal of neural stem cells and the signaling pathways responsible for the proliferation and maintenance of adult stem cells remain largely unknown. In this issue of Molecular Brain [Ma DK et al. Molecular genetic analysis of FGFR1 signaling reveals distinct roles of MAPK and PLCgamma1 activation for self-renewal of adult neural stem cells. Molecular Brain 2009, 2:16], characterized the different roles of MAPK and PLCgamma1 in FGFR1 signaling in the self-renewal of neural stem cells. These novel findi...</description>
            <author>Molecular Brain</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2463693</comments>
            <pubDate>Mon, 08 Jun 2009 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">2463693</guid>        </item>
        <item>
            <title>Molecular genetic analysis of FGFR1 signalling reveals distinct roles of MAPK and PLCg1 activation for self-renewal of adult neural stem cells</title>
            <link>http://www.medworm.com/index.php?rid=2463692&amp;cid=s_37189_168_f&amp;fid=37189&amp;url=http%3A%2F%2Fwww.molecularbrain.com%2Fcontent%2F2%2F1%2F16</link>
            <description>Conclusions:
These studies reveal two amino acid residues in FGFR1 with linked downstream intracellular signal transduction pathways that are essential for maintaining adult NSC self-renewal. The findings provide novel insights into the molecular mechanism regulating adult NSC self-renewal, and pose implications for using these cells in potential therapeutic applications. (Source: Molecular Brain)</description>
            <author>Molecular Brain</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2463692</comments>
            <pubDate>Mon, 08 Jun 2009 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">2463692</guid>        </item>
        <item>
            <title>In vivo multiplex quantitative analysis of 3 forms of alpha melanocyte stimulating hormone in pituitary of prolyl endopeptidase deficient mice.</title>
            <link>http://www.medworm.com/index.php?rid=2457279&amp;cid=s_37189_168_f&amp;fid=37189&amp;url=http%3A%2F%2Fwww.molecularbrain.com%2Fcontent%2F2%2F1%2F14</link>
            <description>Conclusion:
The multiplex targeted quantitative peptidomics technique we present in this study will be decidedly useful to monitor several neuropeptide enzymatic reactions in vivo under varying conditions. (Source: Molecular Brain)</description>
            <author>Molecular Brain</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2457279</comments>
            <pubDate>Tue, 02 Jun 2009 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">2457279</guid>        </item>
        <item>
            <title>Dynamic regulation of RNA editing of ion channels and receptors in the mammalian nervous system</title>
            <link>http://www.medworm.com/index.php?rid=2446537&amp;cid=s_37189_168_f&amp;fid=37189&amp;url=http%3A%2F%2Fwww.molecularbrain.com%2Fcontent%2F2%2F1%2F13</link>
            <description>The post-transcriptional modification of mammalian transcripts in the central nervous system by adenosine-to-inosine RNA editing is an important mechanism for the generation of molecular diversity, and serves to regulate protein function through recoding of genomic information. As the molecular players and an increasing number of edited targets are identified and characterized, adenosine-to-inosine modification serves as an exquisite mechanism for customizing channel function within diverse biological niches. Here, we review the mechanisms that could regulate adenosine-to-inosine RNA editing and the impact of dysregulation in clinical conditions. (Source: Molecular Brain)</description>
            <author>Molecular Brain</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2446537</comments>
            <pubDate>Fri, 29 May 2009 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">2446537</guid>        </item>
        <item>
            <title>Protein synthesis is essential not only for consolidation but also for maintenance and post-retrieval reconsolidation of acrobatic motor skill in rats</title>
            <link>http://www.medworm.com/index.php?rid=2440413&amp;cid=s_37189_168_f&amp;fid=37189&amp;url=http%3A%2F%2Fwww.molecularbrain.com%2Fcontent%2F2%2F1%2F12</link>
            <description>It has been reported that consolidation of motor skill, a type of non-declarative memories, requires protein synthesis, as hippocampus-dependent declarative memory does. However, little is known about the importance of protein synthesis in maintenance and especially post-retrieval reconsolidation of acrobatic motor skill. Here, we show that protein synthesis is essential not only for the consolidation but also for the maintenance and reconsolidation of a rotarod-running skill. Intra-ventricle infusion of the protein synthesis inhibitor anisomycin 0 h but not 2 h post-training caused a severe deficit in the acquisition of the rotarod-running skill. Protein synthesis inhibition (PSI) also caused a deficit in the maintenance of the rotarod-running skill, as well-trained rats demonstrated a de...</description>
            <author>Molecular Brain</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2440413</comments>
            <pubDate>Thu, 28 May 2009 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">2440413</guid>        </item>
        <item>
            <title>Enhanced synaptic long-term potentiation in the anterior cingulate cortex of adult wild mice as compared with that in laboratory mice</title>
            <link>http://www.medworm.com/index.php?rid=2416153&amp;cid=s_37189_168_f&amp;fid=37189&amp;url=http%3A%2F%2Fwww.molecularbrain.com%2Fcontent%2F2%2F1%2F11</link>
            <description>In this report we performed whole-cell patch-clamp recordings from both laboratory wild-type mice and wild mice from a natural environment.  We found that LTP was significantly enhanced in the anterior cingulate cortex (ACC) of the wild mice as compared with that of laboratory mice. In parallel, NMDA receptor NR2B/total NMDA receptor mediated EPSC ratio was significantly increased in slices of wild mice. Our findings provide the first evidence that NMDA NR2B receptors play an important role in experience-dependent synaptic potentiation within the ACC in wild mice as previously reported in laboratory mice. (Source: Molecular Brain)</description>
            <author>Molecular Brain</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2416153</comments>
            <pubDate>Sat, 16 May 2009 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">2416153</guid>        </item>
        <item>
            <title>Sexual attraction enhances glutamate transmission in mammalian anterior cingulate cortex</title>
            <link>http://www.medworm.com/index.php?rid=2397748&amp;cid=s_37189_168_f&amp;fid=37189&amp;url=http%3A%2F%2Fwww.molecularbrain.com%2Fcontent%2F2%2F1%2F9</link>
            <description>Functional brain imaging studies have indicated the essential role of cortical regions, such as the anterior cingulate cortex (ACC), in love and sex. However, the neurobiological basis of how the ACC neurons are activated and engaged in sexual attraction remains unknown. Using transgenic mice in which the expression of green fluorescent protein (GFP) is controlled by the promoter of the activity-dependent gene c-fos, we found that ACC pyramidal neurons are activated by sexual attraction. The presynaptic glutamate release to the activated neurons is increased and pharmacological interventions of transmitter releases or activity in the ACC reduced the interest of male mice to female mice. Our results present a direct evidence of the critical role of the ACC in sexual attraction, with the inc...</description>
            <author>Molecular Brain</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2397748</comments>
            <pubDate>Wed, 06 May 2009 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">2397748</guid>        </item>
        <item>
            <title>Regulation of dopamine transporter activity by carboxypeptidase E</title>
            <link>http://www.medworm.com/index.php?rid=2397747&amp;cid=s_37189_168_f&amp;fid=37189&amp;url=http%3A%2F%2Fwww.molecularbrain.com%2Fcontent%2F2%2F1%2F10</link>
            <description>Conclusion: Taken together, our results reveal a novel role for CPE in the regulation of DAT trafficking and DAT-mediated DA uptake, which may provide a novel target in the treatment of dopamine associated diseases such as drug addiction and obesity. (Source: Molecular Brain)</description>
            <author>Molecular Brain</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2397747</comments>
            <pubDate>Wed, 06 May 2009 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">2397747</guid>        </item>
        <item>
            <title>Tryptophan 2,3-dioxygenase is a key modulator of physiological neurogenesis and anxiety-related behavior in mice</title>
            <link>http://www.medworm.com/index.php?rid=2300770&amp;cid=s_37189_168_f&amp;fid=37189&amp;url=http%3A%2F%2Fwww.molecularbrain.com%2Fcontent%2F2%2F1%2F8</link>
            <description>Although nutrients, including amino acids and their metabolites such as serotonin (5-HT), are strong modulators of anxiety-related behavior, the metabolic pathway(s) responsible for this physiological modulation is not fully understood. Regarding tryptophan (Trp), the initial rate-limiting enzymes for the kynurenine pathway of tryptophan metabolism are tryptophan 2,3-dioxygenase (TDO) and indoleamine 2,3-dioxygenase (IDO). Here, we generated mice deficient for tdo (Tdo-/-). Compared with wild-type littermates, Tdo-/- mice showed increased plasma levels of Trp and its metabolites 5-hydroxyindoleacetic acid (5-HIAA) and kynurenine, as well as increased levels of Trp, 5-HT and 5-HIAA in the hippocampus and midbrain. These mice also showed anxiolytic modulation in the elevated plus maze and op...</description>
            <author>Molecular Brain</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2300770</comments>
            <pubDate>Fri, 27 Mar 2009 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">2300770</guid>        </item>
        <item>
            <title>Requirement of the immediate early gene vesl-1S/homer-1a for fear memory formation</title>
            <link>http://www.medworm.com/index.php?rid=2234826&amp;cid=s_37189_168_f&amp;fid=37189&amp;url=http%3A%2F%2Fwww.molecularbrain.com%2Fcontent%2F2%2F1%2F7</link>
            <description>Conclusions:
These results indicate that the short form of the Vesl family of proteins plays a role in multiple steps of long-term, but not short-term, fear memory formation. (Source: Molecular Brain)</description>
            <author>Molecular Brain</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2234826</comments>
            <pubDate>Thu, 05 Mar 2009 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">2234826</guid>        </item>
        <item>
            <title>Cathepsin D expression level affects alpha-synuclein processing, aggregation, and toxicity in vivo</title>
            <link>http://www.medworm.com/index.php?rid=2170219&amp;cid=s_37189_168_f&amp;fid=37189&amp;url=http%3A%2F%2Fwww.molecularbrain.com%2Fcontent%2F2%2F1%2F5</link>
            <description>Conclusions:
We conclude from these complementary investigations that: one, CathD can effectively degrade excess aSyn in dopaminergic cells; two, ctsd gene mutations result in a lysosomal storage disorder that includes microscopic and biochemical evidence of aSyn misprocessing; and three, CathD deficiency facilitates aSyn toxicity. We therefore postulate that CathD promotes 'synucleinase' activity, and that enhancing its function may lower aSyn concentrations in vivo. (Source: Molecular Brain)</description>
            <author>Molecular Brain</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2170219</comments>
            <pubDate>Mon, 09 Feb 2009 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">2170219</guid>        </item>
        <item>
            <title>Plasticity of NMDA receptor NR2B subunit in memory and chronic pain</title>
            <link>http://www.medworm.com/index.php?rid=2157513&amp;cid=s_37189_168_f&amp;fid=37189&amp;url=http%3A%2F%2Fwww.molecularbrain.com%2Fcontent%2F2%2F1%2F4</link>
            <description>Glutamatergic synapses play critical roles in brain functions and diseases. Long-term potentiation (LTP) is a most effective cellular model for investigating synaptic changes underlie learning as well as brain disease, although different molecular mechanisms are likely involved in LTP in physiological and pathological conditions. In case of learning, N-methyl-D-aspartate (NMDA) receptor is known to be important for triggering learning-related plasticity; alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic (AMPA) receptors are thought to be important for the expression of synaptic changes. In this review, I will review recent evidence on the novel roles of NMDA receptors, in particular NR2B subunit-containing NMDA receptors in learning and chronic pain.   A positive feedback control of NR2B...</description>
            <author>Molecular Brain</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2157513</comments>
            <pubDate>Tue, 03 Feb 2009 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">2157513</guid>        </item>
        <item>
            <title>Effect of ablated hippocampal neurogenesis on the formation and extinction of contextual fear memory</title>
            <link>http://www.medworm.com/index.php?rid=2098459&amp;cid=s_37189_168_f&amp;fid=37189&amp;url=http%3A%2F%2Fwww.molecularbrain.com%2Fcontent%2F2%2F1%2F1</link>
            <description>Newborn neurons in the subgranular zone (SGZ) of the hippocampus incorporate into the dentate gyrus and mature. Numerous studies have focused on hippocampal neurogenesis because of its importance in learning and memory. However, it is largely unknown whether hippocampal neurogenesis is involved in memory extinction per se. Here, we sought to examine the possibility that hippocampal neurogenesis may play a critical role in the formation and extinction of hippocampus-dependent contextual fear memory. By methylazoxymethanol acetate (MAM) or gamma-ray irradiation, hippocampal neurogenesis was impaired in adult mice. Under our experimental conditions, only a severe impairment of hippocampal neurogenesis inhibited the formation of contextual fear memory. However, the extinction of contextual fea...</description>
            <author>Molecular Brain</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2098459</comments>
            <pubDate>Tue, 13 Jan 2009 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">2098459</guid>        </item>
        <item>
            <title>Decreased postnatal neurogenesis in the hippocampus combined with stress experience during adolescence is accompanied by an enhanced incidence of behavioral pathologies in adult mice</title>
            <link>http://www.medworm.com/index.php?rid=2041595&amp;cid=s_37189_168_f&amp;fid=37189&amp;url=http%3A%2F%2Fwww.molecularbrain.com%2Fcontent%2F1%2F1%2F22</link>
            <description>Conclusions:
These results suggest that mice with decreased postnatal neurogenesis during adolescence exhibit vulnerability to stress, and that persistence of this condition may result in decreased activity, and cognitive deficits in adulthood. (Source: Molecular Brain)</description>
            <author>Molecular Brain</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2041595</comments>
            <pubDate>Wed, 17 Dec 2008 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">2041595</guid>        </item>
        <item>
            <title>Normal mitochondrial respiratory function is essential for spatial remote memory in mice</title>
            <link>http://www.medworm.com/index.php?rid=2041596&amp;cid=s_37189_168_f&amp;fid=37189&amp;url=http%3A%2F%2Fwww.molecularbrain.com%2Fcontent%2F1%2F1%2F21</link>
            <description>Conclusion:
Our results indicated that normal mitochondrial respiratory function is necessary for retention and consolidation of memory trace; deficiencies in this function due to high loads of pathogenically mutated mtDNA are responsible for the preferential impairment of spatial remote memory. (Source: Molecular Brain)</description>
            <author>Molecular Brain</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2041596</comments>
            <pubDate>Tue, 16 Dec 2008 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">2041596</guid>        </item>
        <item>
            <title>alpha-Actinin interacts with rapsyn in agrin-stimulated AChR clustering</title>
            <link>http://www.medworm.com/index.php?rid=2007352&amp;cid=s_37189_168_f&amp;fid=37189&amp;url=http%3A%2F%2Fwww.molecularbrain.com%2Fcontent%2F1%2F1%2F18</link>
            <description>AChR is concentrated at the postjunctional membrane at the neuromuscular junction. However, the underlying mechanism is unclear. We show that alpha-actinin, a protein known to cross-link F-actin, interacts with rapsyn, a scaffold protein essential for neuromuscular junction formation. alpha-Actinin, rapsyn, and surface AChR form a ternary complex. Moreover, the rapsyn-alpha-actinin interaction is increased by agrin, a factor known to stimulate AChR clustering. Downregulation of alpha-actinin expression inhibits agrin-mediated AChR clustering. Furthermore, the rapsyn-alpha-actinin interaction can be disrupted by inhibiting Abl and by cholinergic stimulation. Together these results indicate a role for alpha-actinin in AChR clustering. (Source: Molecular Brain)</description>
            <author>Molecular Brain</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2007352</comments>
            <pubDate>Wed, 03 Dec 2008 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">2007352</guid>        </item>
        <item>
            <title>Quantification of gamma-secretase modulation differentiates inhibitor compound selectivity between two substrates Notch and amyloid precursor protein</title>
            <link>http://www.medworm.com/index.php?rid=1934830&amp;cid=s_37189_168_f&amp;fid=37189&amp;url=http%3A%2F%2Fwww.molecularbrain.com%2Fcontent%2F1%2F1%2F15</link>
            <description>Conclusion:
our ELISA-based quantification of Abeta and Nbeta* in combination with the test in zebrafish provides a novel approach for efficient cell-based screening and in vivo validation of APP selective gamma-secretase inhibitors. (Source: Molecular Brain)</description>
            <author>Molecular Brain</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1934830</comments>
            <pubDate>Tue, 04 Nov 2008 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">1934830</guid>        </item>
        <item>
            <title>Development of selective blockers for Ca2+-activated Cl- channel using Xenopus laevis oocytes with an improved drug screening strategy</title>
            <link>http://www.medworm.com/index.php?rid=1915551&amp;cid=s_37189_168_f&amp;fid=37189&amp;url=http%3A%2F%2Fwww.molecularbrain.com%2Fcontent%2F1%2F1%2F14</link>
            <description>Conclusion:
Our results provide an optimal drug screening strategy suitable for high throughput screening, and propose N-(4-trifluoromethylphenyl)anthranilic acid as an improved CaCC blocker. (Source: Molecular Brain)</description>
            <author>Molecular Brain</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1915551</comments>
            <pubDate>Wed, 29 Oct 2008 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">1915551</guid>        </item>
        <item>
            <title>Environmental neurotoxic chemical induces apoptosis in mesencephalic dopaminergic neuronal cells via caspase-3-dependent proteolytic activation of protein kinase Cdelta: Implications for molecular mechanisms of dopaminergic degeneration in Parkinson's disease.</title>
            <link>http://www.medworm.com/index.php?rid=1896442&amp;cid=s_37189_168_f&amp;fid=37189&amp;url=http%3A%2F%2Fwww.molecularbrain.com%2Fcontent%2F1%2F1%2F12</link>
            <description>Conclusions:
Together, we conclude that caspase-3-dependent proteolytic activation of PKCdelta is a critical event in dieldrin-induced apoptotic cell death in dopaminergic neuronal cells. (Source: Molecular Brain)</description>
            <author>Molecular Brain</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1896442</comments>
            <pubDate>Wed, 22 Oct 2008 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">1896442</guid>        </item>
        <item>
            <title>Induction- and conditioning-protocol dependent involvement of NR2B-containing NMDA receptors in synaptic potentiation and contextual fear memory in the hippocampal CA1 region of rats</title>
            <link>http://www.medworm.com/index.php?rid=1892484&amp;cid=s_37189_168_f&amp;fid=37189&amp;url=http%3A%2F%2Fwww.molecularbrain.com%2Fcontent%2F1%2F1%2F9</link>
            <description>Long-term potentiation (LTP) in the hippocampal CA1 region requires the activation of N-methyl-D-aspartate receptors (NMDARs). Studies using genetic and pharmacological approaches have reported inconsistent results of the requirement of NR2B-containing NMDARs in LTP in the CA1 region. Pharmacological studies showed that NR2B-containing NMDARs are not required for LTP, while genetic studies reported that over-expression of NR2B-NMDARs enhances LTP and hippocampus-dependent memory. Here, we provide evidence showing that the functional role of NR2B-NMDARs in hippocampal LTP and memory depends on LTP-inducing and behavior-conditioning protocols. Inhibition of NR2B-NMDARs with the NR2B selective antagonist ifenprodil or Ro25-6981 suppressed LTP induced by spike-timing protocol, with no impact o...</description>
            <author>Molecular Brain</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1892484</comments>
            <pubDate>Tue, 30 Sep 2008 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">1892484</guid>        </item>
        <item>
            <title>Midbrain dopaminergic neuron fate specification: of mice and embryonic stem cells</title>
            <link>http://www.medworm.com/index.php?rid=1838258&amp;cid=s_37189_168_f&amp;fid=37189&amp;url=http%3A%2F%2Fwww.molecularbrain.com%2Fcontent%2F1%2F1%2F8</link>
            <description>The midbrain dopaminergic (mDA) neurons of the substantia nigra and the ventral tegmental area play a fundamental role in the control of voluntary movement and the regulation of emotion, and are severely affected in Parkinson's disease. Recent advances in mouse genetics and vertebrate development have provided us with insight into the genetic cascades involved in the development of mDA neurons, including the induction of mDA neuron progenitors in the ventral mesencephalon, the specification of the mDA neuronal fate and the maintenance of postmitotic mDA neurons. In parallel, rapid progress has been made in the generation of DA neurons from pluripotent stem cells and the development of stem cell-based therapies for Parkinson's disease. Here, we summarize the new findings via the development...</description>
            <author>Molecular Brain</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1838258</comments>
            <pubDate>Tue, 30 Sep 2008 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">1838258</guid>        </item>
        <item>
            <title>Induction- and conditioning-protocol dependent involvement of NR2B-containing NMDA receptors in synaptic potentiation and contextual fear in the hippocampal CA1 region of rats</title>
            <link>http://www.medworm.com/index.php?rid=1838257&amp;cid=s_37189_168_f&amp;fid=37189&amp;url=http%3A%2F%2Fwww.molecularbrain.com%2Fcontent%2F1%2F1%2F9</link>
            <description>Long-term potentiation (LTP) in the hippocampal CA1 region requires the activation of N-methyl-D-aspartate receptors (NMDARs). Studies using genetic and pharmacological approaches have reported inconsistent results of the requirement of NR2B-containing NMDARs in LTP in the CA1 region. Pharmacological studies showed that NR2B-containing NMDARs are not required for LTP, while genetic studies reported that over-expression of NR2B-NMDARs enhances LTP and hippocampus-dependent memory. Here, we provide evidence showing that the functional role of NR2B-NMDARs in hippocampal LTP and memory depends on LTP-inducing and behavior-conditioning protocols. Inhibition of NR2B-NMDARs with the NR2B selective antagonist ifenprodil or Ro25-6981 suppressed LTP induced by spike-timing protocol, with no impact o...</description>
            <author>Molecular Brain</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1838257</comments>
            <pubDate>Tue, 30 Sep 2008 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">1838257</guid>        </item>
        <item>
            <title>Comprehensive behavioral phenotyping of calpastatin-knockout mice</title>
            <link>http://www.medworm.com/index.php?rid=1791956&amp;cid=s_37189_168_f&amp;fid=37189&amp;url=http%3A%2F%2Fwww.molecularbrain.com%2Fcontent%2F1%2F1%2F7</link>
            <description>Conclusions:
These results suggest that calpastatin is likely to be more closely associated with affective rather than cognitive aspects of brain function. (Source: Molecular Brain)</description>
            <author>Molecular Brain</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1791956</comments>
            <pubDate>Mon, 15 Sep 2008 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">1791956</guid>        </item>
        <item>
            <title>Starting at the endophenotype: A role for alpha-CaMKII in schizophrenia?</title>
            <link>http://www.medworm.com/index.php?rid=1783543&amp;cid=s_37189_168_f&amp;fid=37189&amp;url=http%3A%2F%2Fwww.molecularbrain.com%2Fcontent%2F1%2F1%2F5</link>
            <description>Using an endophenotype-driven screen, a new study finds that alpha-calcium/calmodulin kinase II mutant mice exhibit a range of behavioral abnormalities related to schizophrenia. Perhaps most strikingly, this cluster of schizophrenia-related endophenotypes was associated with abnormal neurogenesis in the adult hippocampus, raising the possibility that disrupted adult neurogenesis lies at the core of this and other psychiatric disorders. (Source: Molecular Brain)</description>
            <author>Molecular Brain</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1783543</comments>
            <pubDate>Wed, 10 Sep 2008 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">1783543</guid>        </item>
        <item>
            <title>Atypical evening cortisol profile induces visual recognition memory deficit in healthy human subjects</title>
            <link>http://www.medworm.com/index.php?rid=1721008&amp;cid=s_37189_168_f&amp;fid=37189&amp;url=http%3A%2F%2Fwww.molecularbrain.com%2Fcontent%2F1%2F1%2F4</link>
            <description>Conclusion:
This study suggests that atypical evening salivary cortisol levels have an important role in the early deterioration of recognition memory. The loss of recognition memory, which is vital for everyday life, is a major symptom of the amnesic syndrome and early stages of Alzheimer's disease. Therefore, this study will promote a potential physiologic marker of early deterioration of recognition memory and possible diagnostic strategy for Alzheimer's disease. (Source: Molecular Brain)</description>
            <author>Molecular Brain</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1721008</comments>
            <pubDate>Thu, 21 Aug 2008 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">1721008</guid>        </item>
        <item>
            <title>Welcome to Molecular Brain</title>
            <link>http://www.medworm.com/index.php?rid=1556911&amp;cid=s_37189_168_f&amp;fid=37189&amp;url=http%3A%2F%2Fwww.molecularbrain.com%2Fcontent%2F1%2F1%2F1</link>
            <description>We are delighted to announce the arrival of a brand new journal dedicated to the ever-expanding field of neuroscience. Molecular Brain is a peer-reviewed, open-access online journal that aims at publishing high quality articles as rapidly as possible. The journal will cover a broad spectrum of neuroscience ranging from molecular/cellular to behavioral/cognitive neuroscience and from basic to clinical research. Molecular Brain will publish not only research articles, but also methodology articles, editorials, reviews, and short reports. It will be a premier platform for neuroscientists to exchange their ideas with researchers from around the world to help improve our understanding of the molecular mechanisms of the brain and mind. (Source: Molecular Brain)</description>
            <author>Molecular Brain</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1556911</comments>
            <pubDate>Tue, 17 Jun 2008 04:00:00 +0100</pubDate>
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            <title>Cingulate NMDA NR2B receptors contribute to morphine-induced analgesic tolerance</title>
            <link>http://www.medworm.com/index.php?rid=1556910&amp;cid=s_37189_168_f&amp;fid=37189&amp;url=http%3A%2F%2Fwww.molecularbrain.com%2Fcontent%2F1%2F1%2F2</link>
            <description>This study suggests that selective inhibition of NMDA NR2B receptors may prove useful in combating the development of analgesic tolerance to morphine and proposes a novel role for the ACC in opioid tolerance and morphine induced changes in synaptic plasticity. (Source: Molecular Brain)</description>
            <author>Molecular Brain</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1556910</comments>
            <pubDate>Tue, 17 Jun 2008 04:00:00 +0100</pubDate>
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            <title>Transcriptional regulation of long-term memory in the marine snail Aplysia</title>
            <link>http://www.medworm.com/index.php?rid=1556909&amp;cid=s_37189_168_f&amp;fid=37189&amp;url=http%3A%2F%2Fwww.molecularbrain.com%2Fcontent%2F1%2F1%2F3</link>
            <description>Whereas the induction of short-term memory involves only covalent modifications of constitutively expressed preexisting proteins, the formation of long-term memory requires gene expression, new RNA, and new protein synthesis. On the cellular level, transcriptional regulation is thought to be the starting point for a series of molecular steps necessary for both the initiation and maintenance of long-term synaptic facilitation (LTF). The core molecular features of transcriptional regulation involved in the long-term process are evolutionally conserved in Aplysia, Drosophila, and mouse, and indicate that gene regulation by the cyclic AMP response element binding protein (CREB) acting in conjunction with different combinations of transcriptional factors is critical for the expression of many f...</description>
            <author>Molecular Brain</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=1556909</comments>
            <pubDate>Tue, 17 Jun 2008 04:00:00 +0100</pubDate>
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