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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>Tue, 07 Feb 2012 07:05:45 +0100</lastBuildDate>
        <item>
            <title>Wnt proteins regulate acetylcholine receptor clustering in muscle cells</title>
            <link>http://www.medworm.com/index.php?rid=5665098&amp;cid=s_37189_168_f&amp;fid=37189&amp;url=http%3A%2F%2Fwww.molecularbrain.com%2Fcontent%2F5%2F1%2F7</link>
            <description>Conclusions:
These results identify Wnts as new players in AChR cluster formation, which acts in a manner that requires both MuSK and LRP4, revealing a novel function of LRP4. (Source: Molecular Brain)</description>
            <author>Molecular Brain</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5665098</comments>
            <pubDate>Mon, 06 Feb 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5665098</guid>        </item>
        <item>
            <title>Rapid synaptic potentiation within the anterior cingulate cortex mediates trace fear learning</title>
            <link>http://www.medworm.com/index.php?rid=5657872&amp;cid=s_37189_168_f&amp;fid=37189&amp;url=http%3A%2F%2Fwww.molecularbrain.com%2Fcontent%2F5%2F1%2F6</link>
            <description>Although the cortex has been extensively studied in long-term memory storage, less emphasis has been placed on immediate cortical contributions to fear memory formation. AMPA receptor plasticity is strongly implicated in learning and memory, and studies have identified calcium permeable AMPA receptors (CP-AMPARs) as mediators of synaptic strengthening. Trace fear learning engages the anterior cingulate cortex (ACC), but whether plastic events occur within the ACC in response to trace fear learning, and whether GluN2B subunits are required remains unknown. Here we show that the ACC is necessary for trace fear learning, and shows a rapid 20% upregulation of membrane AMPA receptor GluA1 subunits that is evident immediately after conditioning. Inhibition of NMDA receptor GluN2B subunits during...</description>
            <author>Molecular Brain</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5657872</comments>
            <pubDate>Fri, 03 Feb 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5657872</guid>        </item>
        <item>
            <title>In vivo antinociception of potent mu opioid agonist tetrapeptide analogues and comparison with a compact opioid agonist - neurokinin 1 receptor antagonist chimera</title>
            <link>http://www.medworm.com/index.php?rid=5657873&amp;cid=s_37189_168_f&amp;fid=37189&amp;url=http%3A%2F%2Fwww.molecularbrain.com%2Fcontent%2F5%2F1%2F4</link>
            <description>Conclusions:
We demonstrated that the introduction of a conformational constraint has an important impact on opioid receptor activation and subsequent antinociception in vivo. Further amino acid substitution allowed to identify AN81 as an opioid ligand able to access the CNS and induce antinociception at very low doses (0.1 mg/kg) over a time period up to 7 hours. However, tolerance became apparent after repetitive i.v. administration of the investigated tetrapeptides. This side effect was also observed with the dual opioid agonist-NK1 receptor antagonist SBCHM01. (Source: Molecular Brain)</description>
            <author>Molecular Brain</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5657873</comments>
            <pubDate>Mon, 30 Jan 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5657873</guid>        </item>
        <item>
            <title>Genetic marking and characterization of Tac2-expressing neurons in the central and peripheral nervous system</title>
            <link>http://www.medworm.com/index.php?rid=5626077&amp;cid=s_37189_168_f&amp;fid=37189&amp;url=http%3A%2F%2Fwww.molecularbrain.com%2Fcontent%2F5%2F1%2F3</link>
            <description>Conclusions:
Tac2-Cre mice are a useful tool to mark specific subsets of neurons in the sensory ganglia, the dorsal spinal cord, and the brain. These mice can also be used for future genetic manipulations to study the functions of Tac2-expressing neurons or the functions of genes expressed in these neurons. (Source: Molecular Brain)</description>
            <author>Molecular Brain</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5626077</comments>
            <pubDate>Tue, 24 Jan 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5626077</guid>        </item>
        <item>
            <title>Understanding the physiological roles of the neuronal calcium sensor proteins</title>
            <link>http://www.medworm.com/index.php?rid=5626078&amp;cid=s_37189_168_f&amp;fid=37189&amp;url=http%3A%2F%2Fwww.molecularbrain.com%2Fcontent%2F5%2F1%2F2</link>
            <description>Calcium signalling plays a crucial role in the control of neuronal function and plasticity. Changes in neuronal Ca2+ concentration are detected by Ca2+-binding proteins that can interact with and regulate target proteins to modify their function. Members of the neuronal calcium sensor (NCS) protein family have multiple non-redundant roles in the nervous system. Here we review recent advances in the understanding of the physiological roles of the NCS proteins and the molecular basis for their specificity. (Source: Molecular Brain)</description>
            <author>Molecular Brain</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5626078</comments>
            <pubDate>Mon, 23 Jan 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5626078</guid>        </item>
        <item>
            <title>NMDA Receptor Activation Stimulates Transcription-Independent Rapid Wnt5a Protein Synthesis via the MAPK Signaling Pathway</title>
            <link>http://www.medworm.com/index.php?rid=5570403&amp;cid=s_37189_168_f&amp;fid=37189&amp;url=http%3A%2F%2Fwww.molecularbrain.com%2Fcontent%2F5%2F1%2F1</link>
            <description>Wnt proteins are emerging key regulators of the plasticity and functions of adult brains. However, the mechanisms by which the expression of Wnt proteins is regulated in neurons are unclear. Using primary cortical cultures, we show that activation of NMDA receptors (NMDARs) induces rapid Wnt5a protein synthesis. This NMDAR-regulated Wnt5a synthesis does not require transcription and is a result of activity-dependent translation. We also show that NMDAR-regulated Wnt5a translation depends on MAPK signaling but not mTOR signaling. Our findings suggest that the synaptic activity of CNS neurons activates NMDARs, which in turn stimulate translation from stored Wnt5a mRNA via the MAPK signaling pathway. (Source: Molecular Brain)</description>
            <author>Molecular Brain</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5570403</comments>
            <pubDate>Wed, 04 Jan 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5570403</guid>        </item>
        <item>
            <title>Neuromelanin, neurotransmitter status and brainstem location determine the differential vulnerability of catecholaminergic neurons to mitochondrial DNA deletions</title>
            <link>http://www.medworm.com/index.php?rid=5535259&amp;cid=s_37189_168_f&amp;fid=37189&amp;url=http%3A%2F%2Fwww.molecularbrain.com%2Fcontent%2F4%2F1%2F43</link>
            <description>Conclusions:
Catecholaminergic brainstem neurons are differentially susceptible to mtDNA damage. Pigmented dopaminergic neurons of the SNc show the highest levels of mtDNA deletions, possibly explaining the exceptional vulnerability of the nigro-striatal system in PD and aging. Although loss of pigmented noradrenergic LC neurons also is an early feature of PD pathology, mtDNA deletion levels are not elevated in this nucleus in healthy controls. Thus, mtDNA deletions are neither an inevitable consequence of catecholamine metabolism nor an universal explanation for the regional vulnerability seen in PD. (Source: Molecular Brain)</description>
            <author>Molecular Brain</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5535259</comments>
            <pubDate>Wed, 21 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5535259</guid>        </item>
        <item>
            <title>Dependence of NMDA/GSK3beta Mediated Metaplasticity on TRPM2 Channels at Hippocampal CA3-CA1 Synapses</title>
            <link>http://www.medworm.com/index.php?rid=5535258&amp;cid=s_37189_168_f&amp;fid=37189&amp;url=http%3A%2F%2Fwww.molecularbrain.com%2Fcontent%2F4%2F1%2F44</link>
            <description>Transient receptor potential melastatin 2 (TRPM2) is a calcium permeable non-selective cation channel that functions as a sensor of cellular redox status. Highly expressed within the CNS, we have previously demonstrated the functional expression of these channels in CA1 pyramidal neurons of the hippocampus. Although implicated in oxidative stress-induced neuronal cell death, and potentially in neurodegenerative disease, the physiology of transient receptor potential melastatin 2 channels (TRPM2) is unknown. Interestingly, we have shown that the activation of these channels may be sensitized by co-incident NMDA receptor activation, suggesting a potential contribution of TRPM2 to synaptic transmission. Using hippocampal cultures and slices from TRPM2 null mice we demonstrate that the loss of...</description>
            <author>Molecular Brain</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5535258</comments>
            <pubDate>Wed, 21 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5535258</guid>        </item>
        <item>
            <title>The amount of astrocytic GABA positively correlates with the degree of tonic inhibition in hippocampal CA1 and cerebellum</title>
            <link>http://www.medworm.com/index.php?rid=5438799&amp;cid=s_37189_168_f&amp;fid=37189&amp;url=http%3A%2F%2Fwww.molecularbrain.com%2Fcontent%2F4%2F1%2F42</link>
            <description>In this study, we screened for the presence of astrocytic GABA in various brain regions such as hippocampus, thalamus, hypothalamus and cerebellum using immunohistochemistry. We found that astrocytic GABA was present in the regions that were reported to show tonic inhibition. Because the existence of tonic inhibition in hippocampal CA1 is somewhat controversial, we compared the amount of astrocytic GABA and tonic inhibition between the hippocampal CA1 pyramidal cell layer and the cerebellar granule cell layer. Unlike cerebellar glial cells, hippocampal astrocytes did not contain GABA. The tonic inhibition was also much lower in the pyramidal neurons of hippocampal CA1 compared to the granule cells of cerebellum. Nevertheless, most of the hippocampal astrocytes expressed Bestrophin-1 channe...</description>
            <author>Molecular Brain</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5438799</comments>
            <pubDate>Tue, 22 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5438799</guid>        </item>
        <item>
            <title>Slice orientation and muscarinic acetylcholine receptor activation determine the involvement of N-methyl D-aspartate receptor subunit GluN2B in hippocampal area CA1 long-term depression</title>
            <link>http://www.medworm.com/index.php?rid=5419638&amp;cid=s_37189_168_f&amp;fid=37189&amp;url=http%3A%2F%2Fwww.molecularbrain.com%2Fcontent%2F4%2F1%2F41</link>
            <description>Conclusions:
These results suggest a novel form of NMDAR modulation by mAChRs and clarify some disagreement in the literature. (Source: Molecular Brain)</description>
            <author>Molecular Brain</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5419638</comments>
            <pubDate>Tue, 15 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5419638</guid>        </item>
        <item>
            <title>Regulation of chemotropic guidance of nerve growth cones by microRNA</title>
            <link>http://www.medworm.com/index.php?rid=5378174&amp;cid=s_37189_168_f&amp;fid=37189&amp;url=http%3A%2F%2Fwww.molecularbrain.com%2Fcontent%2F4%2F1%2F40</link>
            <description>Conclusions:
These findings demonstrate a role for miR-134 in translation-dependent guidance of nerve growth cones.  Different guidance cues may act through distinct signaling pathways to elicit PS-dependent and -independent mechanisms to steer growth cones in response to a wide array of spatiotemporal cues during development. (Source: Molecular Brain)</description>
            <author>Molecular Brain</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5378174</comments>
            <pubDate>Thu, 03 Nov 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5378174</guid>        </item>
        <item>
            <title>DIP/WISH deficiency enhances synaptic function and performance in the Barnes maze</title>
            <link>http://www.medworm.com/index.php?rid=5344828&amp;cid=s_37189_168_f&amp;fid=37189&amp;url=http%3A%2F%2Fwww.molecularbrain.com%2Fcontent%2F4%2F1%2F39</link>
            <description>Conclusions:
We conclude that DIP/WISH deletion improves performance in the Barnes maze test in mice probably through increased hippocampal long-term potentiation. (Source: Molecular Brain)</description>
            <author>Molecular Brain</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5344828</comments>
            <pubDate>Fri, 21 Oct 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5344828</guid>        </item>
        <item>
            <title>Automated 4D analysis of dendritic spine morphology: applications to stimulus-induced spine remodeling and pharmacological rescue in a disease model</title>
            <link>http://www.medworm.com/index.php?rid=5294712&amp;cid=s_37189_168_f&amp;fid=37189&amp;url=http%3A%2F%2Fwww.molecularbrain.com%2Fcontent%2F4%2F1%2F38</link>
            <description>Uncovering the mechanisms that regulate dendritic spine morphology has been limited, in part, by the lack of efficient and unbiased methods for analyzing spines. Here, we describe an automated 3D spine morphometry method and its application to spine remodeling in live neurons and spine abnormalities in a disease model. We anticipate that this approach will advance studies of synapse structure and function in brain development, plasticity, and disease. (Source: Molecular Brain)</description>
            <author>Molecular Brain</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5294712</comments>
            <pubDate>Fri, 07 Oct 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5294712</guid>        </item>
        <item>
            <title>ESCRT-III subunits Snf7-1 and Snf7-2 differentially regulate transmembrane cargos in hESC-derived human neurons</title>
            <link>http://www.medworm.com/index.php?rid=5294713&amp;cid=s_37189_168_f&amp;fid=37189&amp;url=http%3A%2F%2Fwww.molecularbrain.com%2Fcontent%2F4%2F1%2F37</link>
            <description>Conclusion:
These findings indicate that different mammalian paralogs of the yeast ESCRT-III subunit Snf7 have non-redundant functions in human neurons, suggesting that ESCRT-III with distinct subunit compositions may preferentially regulate different cargo proteins. (Source: Molecular Brain)</description>
            <author>Molecular Brain</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5294713</comments>
            <pubDate>Wed, 05 Oct 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5294713</guid>        </item>
        <item>
            <title>Imaging synaptic plasticity</title>
            <link>http://www.medworm.com/index.php?rid=5270951&amp;cid=s_37189_168_f&amp;fid=37189&amp;url=http%3A%2F%2Fwww.molecularbrain.com%2Fcontent%2F4%2F1%2F36</link>
            <description>Over the past decade, the use and development of optical imaging techniques has advanced our understanding of synaptic plasticity by offering the spatial and temporal resolution necessary to examine long-term changes at individual synapses. Here, we review the use of these techniques in recent studies of synaptic plasticity and, in particular, of long-term potentiation in the hippocampus. (Source: Molecular Brain)</description>
            <author>Molecular Brain</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5270951</comments>
            <pubDate>Thu, 29 Sep 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5270951</guid>        </item>
        <item>
            <title>Transplantation of human neural stem/progenitor cells overexpressing Galectin-1 improves functional recovery from focal brain ischemia in the Mongolian gerbil</title>
            <link>http://www.medworm.com/index.php?rid=5258258&amp;cid=s_37189_168_f&amp;fid=37189&amp;url=http%3A%2F%2Fwww.molecularbrain.com%2Fcontent%2F4%2F1%2F35</link>
            <description>This study provides evidence for a potential application of hGal1 with hNSPCs-transplantation in the treatment of brain ischemia. (Source: Molecular Brain)</description>
            <author>Molecular Brain</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5258258</comments>
            <pubDate>Tue, 27 Sep 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5258258</guid>        </item>
        <item>
            <title>The dual origin of the peripheral olfactory system: placode and neural crest</title>
            <link>http://www.medworm.com/index.php?rid=5247666&amp;cid=s_37189_168_f&amp;fid=37189&amp;url=http%3A%2F%2Fwww.molecularbrain.com%2Fcontent%2F4%2F1%2F34</link>
            <description>Conclusion:
Our data demonstrates that the NC plays a larger role in the development of the olfactory system than previously believed, and suggests that NC-derived cells may in part be responsible for the remarkable capacity of the OE for neurogenesis and regeneration. (Source: Molecular Brain)</description>
            <author>Molecular Brain</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5247666</comments>
            <pubDate>Fri, 23 Sep 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5247666</guid>        </item>
        <item>
            <title>Impaired spatial and contextual memory formation in galectin-1 deficient mice</title>
            <link>http://www.medworm.com/index.php?rid=5181024&amp;cid=s_37189_168_f&amp;fid=37189&amp;url=http%3A%2F%2Fwww.molecularbrain.com%2Fcontent%2F4%2F1%2F33</link>
            <description>Galectins are a 15 member family of carbohydrate-binding proteins that have been implicated in cancer, immunity, inflammation and development. While galectins are expressed in the central nervous system, little is known about their function in the adult brain. Previously we have shown that galectin-1 (gal-1) is expressed in the adult hippocampus, and, in particular, in putative neural stem cells in the subgranular zone. To evaluate how gal-1 might contribute to hippocampal memory function here we studied galectin-1 null mutant (gal-1-/-) mice. Compared to their wildtype littermate controls, gal-1-/- mice exhibited impaired spatial learning in the water maze and contextual fear learning. Interestingly, tone fear conditioning was normal in gal-1-/- mice suggesting that loss of gal-1 might es...</description>
            <author>Molecular Brain</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5181024</comments>
            <pubDate>Wed, 31 Aug 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5181024</guid>        </item>
        <item>
            <title>Neuronal and microglial mechanisms of neuropathic pain</title>
            <link>http://www.medworm.com/index.php?rid=5077367&amp;cid=s_37189_168_f&amp;fid=37189&amp;url=http%3A%2F%2Fwww.molecularbrain.com%2Fcontent%2F4%2F1%2F31</link>
            <description>${item.shortDescription} (Source: Molecular Brain)</description>
            <author>Molecular Brain</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5077367</comments>
            <pubDate>Fri, 29 Jul 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5077367</guid>        </item>
        <item>
            <title>Differential trafficking of AMPA receptors following activation of NMDA receptors and mGluRs</title>
            <link>http://www.medworm.com/index.php?rid=5069163&amp;cid=s_37189_168_f&amp;fid=37189&amp;url=http%3A%2F%2Fwww.molecularbrain.com%2Fcontent%2F4%2F1%2F30</link>
            <description>${item.shortDescription} (Source: Molecular Brain)</description>
            <author>Molecular Brain</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5069163</comments>
            <pubDate>Tue, 26 Jul 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5069163</guid>        </item>
        <item>
            <title>Fetal alcohol exposure leads to abnormal olfactory bulb development and impaired odor discrimination in adult mice.</title>
            <link>http://www.medworm.com/index.php?rid=5007667&amp;cid=s_37189_168_f&amp;fid=37189&amp;url=http%3A%2F%2Fwww.molecularbrain.com%2Fcontent%2F4%2F1%2F29</link>
            <description>Conclusions: Using a combination of techniques, including structural brain imaging, in vitro and in vivo cell detection methods, and behavioral testing, we found that fetal alcohol exposure results in smaller olfactory bulbs and impairments in odor discrimination that persist into adulthood. Furthermore, we found that these abnormalities in olfactory bulb structure and function may arise from deficits in the generation of new olfactory bulb neurons during early postnatal development. (Source: Molecular Brain)</description>
            <author>Molecular Brain</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5007667</comments>
            <pubDate>Wed, 06 Jul 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5007667</guid>        </item>
        <item>
            <title>Long-term changes of spine dynamics and microglia after transient peripheral immune response triggered by LPS in vivo</title>
            <link>http://www.medworm.com/index.php?rid=4944786&amp;cid=s_37189_168_f&amp;fid=37189&amp;url=http%3A%2F%2Fwww.molecularbrain.com%2Fcontent%2F4%2F1%2F27</link>
            <description>Conclusions:
These results indicate long-lasting aggravating effects of a single transient peripheral immune response on both spines and microglia. The parallel persistent alterations of both spine turnover and the state of microglia in vivo suggest the presence of a pathological mechanism that sustains the enhanced remodeling of neural networks weeks after peripheral immune responses. This pathological mechanism may also underlie long-lasting cognitive dysfunctions after septic encephalopathy in human patients. (Source: Molecular Brain)</description>
            <author>Molecular Brain</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4944786</comments>
            <pubDate>Thu, 16 Jun 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4944786</guid>        </item>
        <item>
            <title>Regulation of opioid receptor signalling: implications for the development of analgesic tolerance</title>
            <link>http://www.medworm.com/index.php?rid=4933511&amp;cid=s_37189_168_f&amp;fid=37189&amp;url=http%3A%2F%2Fwww.molecularbrain.com%2Fcontent%2F4%2F1%2F25</link>
            <description>Opiate drugs are the most effective analgesics available but their clinical use is restricted by severe side effects. Some of these undesired actions appear after repeated administration and are related to adaptive changes directed at counteracting the consequences of sustained opioid receptor activation. Here we will discuss adaptations that contribute to the development of tolerance. The focus of the first part of the review is set on molecular mechanisms involved in the regulation of opioid receptor signalling in heterologous expression systems and neurons. In the second part we assess how adaptations that take place in vivo may contribute to analgesic tolerance developed during repeated opioid administration. (Source: Molecular Brain)</description>
            <author>Molecular Brain</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4933511</comments>
            <pubDate>Sun, 12 Jun 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4933511</guid>        </item>
        <item>
            <title>Dopamine D1-D2 receptor heteromer signaling pathway in brain: Emerging physiological relevance</title>
            <link>http://www.medworm.com/index.php?rid=4933510&amp;cid=s_37189_168_f&amp;fid=37189&amp;url=http%3A%2F%2Fwww.molecularbrain.com%2Fcontent%2F4%2F1%2F26</link>
            <description>Dopamine is an important catecholamine neurotransmitter modulating many physiological functions, and is linked to psychopathology of many diseases such as schizophrenia and drug addiction. Dopamine D1 and D2 receptors are the most abundant dopaminergic receptors in the striatum, and although a clear segregation between the pathways expressing these two receptors has been reported in certain subregions, the presence of D1-D2 receptor heteromers within a unique subset of neurons, forming a novel signal transducing functional entity has been shown. Recently, significant progress has been made in elucidating the signaling pathways activated by the D1-D2 receptor heteromer and their potential physiological relevance. (Source: Molecular Brain)</description>
            <author>Molecular Brain</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4933510</comments>
            <pubDate>Sun, 12 Jun 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4933510</guid>        </item>
        <item>
            <title>Copy number loss of (Src homology 2 domain containing)-transforming protein 2 (SHC2) gene: Discordant loss in monozygotic twins and frequent loss in patients with multiple system atrophy</title>
            <link>http://www.medworm.com/index.php?rid=4920847&amp;cid=s_37189_168_f&amp;fid=37189&amp;url=http%3A%2F%2Fwww.molecularbrain.com%2Fcontent%2F4%2F1%2F24</link>
            <description>Conclusions:
Copy number loss of SHC2 strongly indicates a causal link to MSA. CNV analysis of phenotypically discordant MZ twins is a powerful tool for identifying disease-predisposing loci. Our results would enable the identification of novel diagnostic measure, therapeutic targets and better understanding of the etiology of MSA. (Source: Molecular Brain)</description>
            <author>Molecular Brain</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4920847</comments>
            <pubDate>Thu, 09 Jun 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4920847</guid>        </item>
        <item>
            <title>mRNA binding protein Staufen 1-dependent regulation of pyramidal cell spine morphology via NMDA receptor-mediated synaptic plasticity</title>
            <link>http://www.medworm.com/index.php?rid=4892312&amp;cid=s_37189_168_f&amp;fid=37189&amp;url=http%3A%2F%2Fwww.molecularbrain.com%2Fcontent%2F4%2F1%2F22</link>
            <description>Staufens (Stau) are RNA-binding proteins involved in mRNA transport, localization, decay and translational control. The Staufen 1 (Stau1) isoform was recently identified as necessary for the protein synthesis-dependent late phase long-term potentiation (late-LTP) and for the maintenance of mature dendritic spines and synaptic activity in hippocampal CA1 pyramidal cells, strongly suggesting a role of mRNA regulation by Stau1 in these processes. However, the causal relationship between these impairments in synaptic function (spine shape and basal synaptic activity) and plasticity (late-LTP) remains unclear. Here, we determine that the effects of Stau1 knockdown on spine shape and size are mimicked by blocking NMDA receptors (or elevating extracellular Mg2+) and that Stau1 knockdown in the pr...</description>
            <author>Molecular Brain</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4892312</comments>
            <pubDate>Wed, 01 Jun 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4892312</guid>        </item>
        <item>
            <title>GPCR oligomers in pharmacology and signaling</title>
            <link>http://www.medworm.com/index.php?rid=4871694&amp;cid=s_37189_168_f&amp;fid=37189&amp;url=http%3A%2F%2Fwww.molecularbrain.com%2Fcontent%2F4%2F1%2F20</link>
            <description>G protein-coupled receptors (GPCRs) represent one of the largest families of cell surface receptors, and are the target of more than half of the current therapeutic drugs on the market. When activated by an agonist, the GPCR undergoes conformational changes that facilitate its interaction with heterotrimeric G proteins, which then relay signals to downstream intracellular effectors. Although GPCRs were thought to function as monomers, many studies support the hypothesis that G protein coupling involves the formation of GPCR homo- and/or hetero-complexes. These complex systems have been suggested to exhibit specific signaling cascades, pharmacological, internalization, and recycling properties. In this review, we summarize recent advances in our understanding of the structure, function and ...</description>
            <author>Molecular Brain</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4871694</comments>
            <pubDate>Thu, 26 May 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4871694</guid>        </item>
        <item>
            <title>Transcriptional dysregulation of 5-HT1A autoreceptors in mental illness</title>
            <link>http://www.medworm.com/index.php?rid=4871693&amp;cid=s_37189_168_f&amp;fid=37189&amp;url=http%3A%2F%2Fwww.molecularbrain.com%2Fcontent%2F4%2F1%2F21</link>
            <description>The serotonin-1A (5-HT1A) receptor is among the most abundant and widely distributed 5-HT receptors in the brain, but is also expressed on serotonin neurons as an autoreceptor where it plays a critical role in regulating the activity of the entire serotonin system. Over-expression of the 5-HT1A autoreceptor has been implicated in reducing serotonergic neurotransmission, and is associated with major depression and suicide. Extensive characterization of the transcriptional regulation of the 5-HT1A gene (HTR1A) using cell culture systems has revealed a GC-rich &quot;housekeeping&quot; promoter that non-selectively drives its expression; this is flanked by a series of upstream repressor elements for REST, Freud-1/CC2D1A and Freud-2/CC2D1B factors that not only restrict its expression to neurons, but may...</description>
            <author>Molecular Brain</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4871693</comments>
            <pubDate>Thu, 26 May 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4871693</guid>        </item>
        <item>
            <title>Physiological synaptic signals initiate sequential spikes at soma of cortical pyramidal neurons</title>
            <link>http://www.medworm.com/index.php?rid=4802064&amp;cid=s_37189_168_f&amp;fid=37189&amp;url=http%3A%2F%2Fwww.molecularbrain.com%2Fcontent%2F4%2F1%2F19</link>
            <description>The neurons in the brain produce sequential spikes as the digital codes whose various patterns manage well-organized cognitions and behaviors. A source for the physiologically integrated synaptic signals to initiate digital spikes remains unknown, which we studied at pyramidal neurons of cortical slices. In dual recordings from the soma vs. axon, the signals recorded in vivo induce somatic spikes with higher capacity, which is associated with lower somatic thresholds and shorter refractory periods mediated by voltage-gated sodium channels. The introduction of these parameters from the soma and axon into NEURON model simulates sequential spikes being somatic in origin. Physiological signals integrated from synaptic inputs primarily trigger the soma to encode neuronal digital spikes. (Source...</description>
            <author>Molecular Brain</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4802064</comments>
            <pubDate>Sat, 07 May 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4802064</guid>        </item>
        <item>
            <title>A human-mouse conserved sex bias in amygdala gene expression related to circadian clock and energy metabolism</title>
            <link>http://www.medworm.com/index.php?rid=4788837&amp;cid=s_37189_168_f&amp;fid=37189&amp;url=http%3A%2F%2Fwww.molecularbrain.com%2Fcontent%2F4%2F1%2F18</link>
            <description>Conclusions:
These results suggest that the basolateral amygdala is a sexually dimorphic structure, featuring a regulatory cascade of mitochondrial function and circadian rhythm, potentially linked through sirtuins and hormone nuclear receptors. Hence, baseline differences in amygdalar circadian regulation of cellular metabolism may contribute to sex-related differences in mood regulation and vulnerability to major depression. (Source: Molecular Brain)</description>
            <author>Molecular Brain</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4788837</comments>
            <pubDate>Tue, 03 May 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4788837</guid>        </item>
        <item>
            <title>Genome-wide screen for modifiers of Parkinson's disease genes in Drosophila</title>
            <link>http://www.medworm.com/index.php?rid=4733548&amp;cid=s_37189_168_f&amp;fid=37189&amp;url=http%3A%2F%2Fwww.molecularbrain.com%2Fcontent%2F4%2F1%2F17</link>
            <description>Conclusions:
We took an unbiased genetic approach to systematically isolate modifiers of PD genes in Drosophila. Further study of novel PD-interacting genes will shed new light on the function of PD genes and help in the development of new therapeutic strategies for treating Parkinson's disease. (Source: Molecular Brain)</description>
            <author>Molecular Brain</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4733548</comments>
            <pubDate>Mon, 18 Apr 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4733548</guid>        </item>
        <item>
            <title>Opposing Roles of PlexinA and PlexinB in Axonal Branch and Varicosity Formation</title>
            <link>http://www.medworm.com/index.php?rid=4709035&amp;cid=s_37189_168_f&amp;fid=37189&amp;url=http%3A%2F%2Fwww.molecularbrain.com%2Fcontent%2F4%2F1%2F15</link>
            <description>Establishing precise synaptic connectivity during development is crucial for neural circuit function. However, very few molecules have been identified that are involved in determining where and how many synapses form. The Plexin cell-surface molecules are a conserved family of axon guidance receptors that mediate axon fasciculation and repulsion during neural development, and later in development PlexinA receptors are involved in eliminating axonal branches and synapse numbers. Here we investigate the roles of PlexinA and PlexinB receptors in axonal branch and axonal varicosity formation in Drosophila. We knocked down PlexinA or PlexinB expression using RNAi in identified mechanosensory neurons and analyzed axonal branching patterns and varicosity formations. Reducing PlexinA expression in...</description>
            <author>Molecular Brain</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4709035</comments>
            <pubDate>Tue, 12 Apr 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4709035</guid>        </item>
        <item>
            <title>A Co-operative Regulation of Neuronal Excitability by UNC-7 Innexin and NCA/NALCN Leak Channel</title>
            <link>http://www.medworm.com/index.php?rid=4709034&amp;cid=s_37189_168_f&amp;fid=37189&amp;url=http%3A%2F%2Fwww.molecularbrain.com%2Fcontent%2F4%2F1%2F16</link>
            <description>Gap junctions mediate the electrical coupling and intercellular communication between neighboring cells. Some gap junction proteins, namely connexins and pannexins in vertebrates, and innexins in invertebrates, may also function as hemichannels. A conserved NCA/Dma1U/NALCN family cation leak channel regulates the excitability and activity of vertebrate and invertebrate neurons. In the present study, we describe a genetic and functional interaction between the innexin UNC-7 and the cation leak channel NCA in Caenorhabditis elegans neurons. While the loss of the neuronal NCA channel function leads to a reduced evoked postsynaptic current at neuromuscular junctions, a simultaneous loss of the UNC-7 function restores the evoked response. The expression of UNC-7 in neurons reverts the effect of...</description>
            <author>Molecular Brain</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4709034</comments>
            <pubDate>Tue, 12 Apr 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4709034</guid>        </item>
        <item>
            <title>Identification of a Novel Intronic Enhancer Responsible for the
Transcriptional Regulation of Musashi1 in Neural Stem/Progenitor
Cells</title>
            <link>http://www.medworm.com/index.php?rid=4704383&amp;cid=s_37189_168_f&amp;fid=37189&amp;url=http%3A%2F%2Fwww.molecularbrain.com%2Fcontent%2F4%2F1%2F14</link>
            <description>Conclusions:
A regulatory element for Msi1 transcription in NS/PCs is located in the sixth intron of the Msi1 gene. The 595-bp D5E2 intronic enhancer can transactivate Msi1 gene expression with cell-type specificity markedly similar to the endogenous Msi1 expression patterns. (Source: Molecular Brain)</description>
            <author>Molecular Brain</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4704383</comments>
            <pubDate>Tue, 12 Apr 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4704383</guid>        </item>
        <item>
            <title>si-RNA inhibition of brain insulin or insulin-like growth factor receptors causes developmental cerebellar abnormalities: relevance to fetal alcohol spectrum disorder</title>
            <link>http://www.medworm.com/index.php?rid=4642293&amp;cid=s_37189_168_f&amp;fid=37189&amp;url=http%3A%2F%2Fwww.molecularbrain.com%2Fcontent%2F4%2F1%2F13</link>
            <description>Conclusions: early postnatal inhibition of brain InR expression, and to lesser extents, IGF-R, causes structural and functional abnormalities that resemble effects of FASD. The findings suggest that major abnormalities in brains with FASD are mediated by impairments in insulin/IGF signaling. Potential therapeutic strategies to reduce the long-term impact of prenatal alcohol exposure may include treatment with agents that restore brain insulin and IGF responsiveness. (Source: Molecular Brain)</description>
            <author>Molecular Brain</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4642293</comments>
            <pubDate>Sun, 27 Mar 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4642293</guid>        </item>
        <item>
            <title>Behavioral destabilization induced by the selective serotonin reuptake inhibitor fluoxetine</title>
            <link>http://www.medworm.com/index.php?rid=4600330&amp;cid=s_37189_168_f&amp;fid=37189&amp;url=http%3A%2F%2Fwww.molecularbrain.com%2Fcontent%2F4%2F1%2F12</link>
            <description>Conclusions:
Our results demonstrate that the SSRI fluoxetine can induce marked day-to-day changes in activity levels of mice in the familiar environment, and that the dematuration of the hippocampal granule cells is closely associated with the expression of this destabilized behavior. Based on these results, we propose that the granule cell dematuration can be a potential cellular basis underlying switching-like changes in the behavioral state associated with SSRI treatments. (Source: Molecular Brain)</description>
            <author>Molecular Brain</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4600330</comments>
            <pubDate>Wed, 16 Mar 2011 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4600330</guid>        </item>
        <item>
            <title>Activity-dependent brain-derived neurotrophic factor expression regulates cortistatin-interneurons and sleep behavior</title>
            <link>http://www.medworm.com/index.php?rid=4565723&amp;cid=s_37189_168_f&amp;fid=37189&amp;url=http%3A%2F%2Fwww.molecularbrain.com%2Fcontent%2F4%2F1%2F11</link>
            <description>Conclusion:
Our studies suggest that regulation of cortistatin-expressing interneurons by activity-dependent BDNF expression may contribute to regulation of sleep behavior. (Source: Molecular Brain)</description>
            <author>Molecular Brain</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4565723</comments>
            <pubDate>Wed, 09 Mar 2011 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4565723</guid>        </item>
        <item>
            <title>Chronic treatment with fluoxetine for more than 6 weeks decreases neurogenesis in the subventricular zone of adult mice</title>
            <link>http://www.medworm.com/index.php?rid=4559966&amp;cid=s_37189_168_f&amp;fid=37189&amp;url=http%3A%2F%2Fwww.molecularbrain.com%2Fcontent%2F4%2F1%2F10</link>
            <description>Conclusions:
These results demonstrate that long-term (more than 6 weeks) treatment with FLX has the opposite effect on neurogenesis in the SVZ than it does in the DG. The results also suggest that the decrease in neurogenesis in the SVZ might be involved in some aspects of the drugs' therapeutic effects on depression. In addition, our findings raise the possibility that some of the side effects of antidepressants might be mediated by decreased adult neurogenesis in the SVZ. (Source: Molecular Brain)</description>
            <author>Molecular Brain</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4559966</comments>
            <pubDate>Tue, 08 Mar 2011 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4559966</guid>        </item>
        <item>
            <title>Molecular mechanisms for the destabilization and restabilization of reactivated spatial memory in the Morris water maze</title>
            <link>http://www.medworm.com/index.php?rid=4464341&amp;cid=s_37189_168_f&amp;fid=37189&amp;url=http%3A%2F%2Fwww.molecularbrain.com%2Fcontent%2F4%2F1%2F9</link>
            <description>Conclusions:
Our findings indicated that the reactivated spatial memory is destabilized through the activation of CB1 and LVGCCs and then restabilized through the activation of NMDAR- and CREB-mediated transcription. We also suggest that the reactivated spatial memory undergoes destabilization and restabilization in the hippocampus, through similar molecular processes as those for reactivated contextual fear memories, which require CB1 and LVGCCs for destabilization and NMDAR and CREB for restabilization. (Source: Molecular Brain)</description>
            <author>Molecular Brain</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4464341</comments>
            <pubDate>Fri, 11 Feb 2011 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4464341</guid>        </item>
        <item>
            <title>Properties of Contextual Memory Formed in the Absence of alphaCaMKII Autophosphorylation</title>
            <link>http://www.medworm.com/index.php?rid=4411403&amp;cid=s_37189_168_f&amp;fid=37189&amp;url=http%3A%2F%2Fwww.molecularbrain.com%2Fcontent%2F4%2F1%2F8</link>
            <description>The alpha-isoform of calcium/calmodulin-dependent kinase II (alphaCaMKII) is a major synaptic kinase that undergoes autophosphorylation after NMDA receptor activation, switching the kinase into a calcium-independent activity state. This alphaCaMKII autophosphorylation is essential for NMDA receptor-dependent long-term potentiation (LTP), induced by a single tetanus, in hippocampal area CA1 and in neocortex. Furthermore, the alphaCaMKII autophosphorylation is essential for contextual long-term memory (LTM) formation after a single training trial but not after a massed training session. Here, we show that in the absence of alphaCaMKII autophosphorylation contextual fear conditioning is hippocampus dependent and that multi-tetanus-dependent late-LTP cannot be induced in hippocampal area CA1. ...</description>
            <author>Molecular Brain</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4411403</comments>
            <pubDate>Fri, 28 Jan 2011 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4411403</guid>        </item>
        <item>
            <title>Galectin-1 is expressed in early-type neural progenitor cells and down-regulates neurogenesis in the adult hippocampus</title>
            <link>http://www.medworm.com/index.php?rid=4405444&amp;cid=s_37189_168_f&amp;fid=37189&amp;url=http%3A%2F%2Fwww.molecularbrain.com%2Fcontent%2F4%2F1%2F7</link>
            <description>Conclusions:
Galectin-1 is expressed in the neural stem cells and down-regulates neurogenesis in the adult hippocampus. (Source: Molecular Brain)</description>
            <author>Molecular Brain</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4405444</comments>
            <pubDate>Thu, 27 Jan 2011 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4405444</guid>        </item>
        <item>
            <title>Induction and requirement of gene expression in the anterior cingulate cortex and medial prefrontal cortex for the consolidation of inhibitory avoidance memory</title>
            <link>http://www.medworm.com/index.php?rid=4371683&amp;cid=s_37189_168_f&amp;fid=37189&amp;url=http%3A%2F%2Fwww.molecularbrain.com%2Fcontent%2F4%2F1%2F4</link>
            <description>Conclusion:
Our observations indicated that the formation of IA memory requires gene expression in the ACC and mPFC as well as in the amygdala and hippocampus, suggesting essential roles of the ACC and mPFC in IA memory formation. (Source: Molecular Brain)</description>
            <author>Molecular Brain</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4371683</comments>
            <pubDate>Wed, 19 Jan 2011 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4371683</guid>        </item>
        <item>
            <title>DNA methylation-mediated control of learning and memory</title>
            <link>http://www.medworm.com/index.php?rid=4371682&amp;cid=s_37189_168_f&amp;fid=37189&amp;url=http%3A%2F%2Fwww.molecularbrain.com%2Fcontent%2F4%2F1%2F5</link>
            <description>Animals constantly receive and respond to external or internal stimuli, and these experiences are learned and memorized in their brains. In animals, this is a crucial feature for survival, by making it possible for them to adapt their behavioral patterns to the ever-changing environment. For this learning and memory process, nerve cells in the brain undergo enormous molecular and cellular changes, not only in the input-output-related local subcellular compartments but also in the central nucleus. Interestingly, the DNA methylation pattern, which is normally stable in a terminally differentiated cell and defines the cell type identity, is emerging as an important regulatory mechanism of behavioral plasticity. The elucidation of how this covalent modification of DNA, which is known to be the...</description>
            <author>Molecular Brain</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4371682</comments>
            <pubDate>Wed, 19 Jan 2011 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4371682</guid>        </item>
        <item>
            <title>Directed evolution of a three-finger neurotoxin by using cDNA display yields antagonists as well as agonists of interleukin-6 receptor signaling</title>
            <link>http://www.medworm.com/index.php?rid=4322339&amp;cid=s_37189_168_f&amp;fid=37189&amp;url=http%3A%2F%2Fwww.molecularbrain.com%2Fcontent%2F4%2F1%2F2</link>
            <description>Conclusions:
This study shows 3F protein is amenable to introduce amino acid changes in the loops that enable preparation of a high diversity library that can be utilized to obtain ligands against macromolecules. We believe this is the first report of protein engineering to convert a neurotoxin to receptor ligands other than the parent receptor, the identification of an agonist from non-immunoglobulin proteins, the construction of peptide mimic of IL-6, and the successful size reduction of a single-chain protein. (Source: Molecular Brain)</description>
            <author>Molecular Brain</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4322339</comments>
            <pubDate>Fri, 07 Jan 2011 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4322339</guid>        </item>
        <item>
            <title>Presynaptic protein synthesis required for NT-3-induced long-term synaptic modulation</title>
            <link>http://www.medworm.com/index.php?rid=4318134&amp;cid=s_37189_168_f&amp;fid=37189&amp;url=http%3A%2F%2Fwww.molecularbrain.com%2Fcontent%2F4%2F1%2F1</link>
            <description>Conclusions:
Our results provide mechanistic insights into the cell-specific requirement for protein synthesis in the long-term synaptic modulation by neurotrophins. The GyrB-PKR system may be useful tool to study protein synthesis in a cell-specific manner. (Source: Molecular Brain)</description>
            <author>Molecular Brain</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4318134</comments>
            <pubDate>Fri, 07 Jan 2011 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4318134</guid>        </item>
        <item>
            <title>The physiological roles of vesicular GABA transporter during embryonic development: a study using knockout mice</title>
            <link>http://www.medworm.com/index.php?rid=4298516&amp;cid=s_37189_168_f&amp;fid=37189&amp;url=http%3A%2F%2Fwww.molecularbrain.com%2Fcontent%2F3%2F1%2F40</link>
            <description>Conclusion:
VGAT is fundamental for the GABA- and/or glycine-mediated transmission that supports embryonic development. VGAT knockout mice will be useful for further investigating the roles of VGAT in normal physiology and pathophysiologic processes. (Source: Molecular Brain)</description>
            <author>Molecular Brain</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4298516</comments>
            <pubDate>Thu, 30 Dec 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4298516</guid>        </item>
        <item>
            <title>PICK1 regulates the trafficking of ASIC1a and acidotoxicity in a BAR domain lipid binding-dependent manner</title>
            <link>http://www.medworm.com/index.php?rid=4277725&amp;cid=s_37189_168_f&amp;fid=37189&amp;url=http%3A%2F%2Fwww.molecularbrain.com%2Fcontent%2F3%2F1%2F39</link>
            <description>Conclusions:
Taken together, our results indicate that PICK1 regulates trafficking and function of ASIC1a in a lipid binding-dependent manner. (Source: Molecular Brain)</description>
            <author>Molecular Brain</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4277725</comments>
            <pubDate>Tue, 21 Dec 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4277725</guid>        </item>
        <item>
            <title>The modulation of TRPM7 currents by nafamostat mesilate depends directly upon extracellular concentrations of divalent cations</title>
            <link>http://www.medworm.com/index.php?rid=4219520&amp;cid=s_37189_168_f&amp;fid=37189&amp;url=http%3A%2F%2Fwww.molecularbrain.com%2Fcontent%2F3%2F1%2F38</link>
            <description>Concentrations of extracellular divalent cations (Ca2+ and Mg2+) fall substantially during intensive synaptic transmission as well as during some pathophysiological conditions such as epilepsy and brain ischemia. Here we report that a synthetic serine protease inhibitor, nafamostat mesylate (NM), and several of its analogues, block recombinant TRPM7 currents expressed in HEK293T cells in inverse relationship to the concentration of extracellular divalent cations. Lowering extracellular Ca2+ and Mg2+ also evokes a divalent-sensitive non-selective cation current that is mediated by TRPM7 expression in hippocampal neurons. In cultured hippocampal neurons, NM blocked these TRPM7-mediated currents with an apparent affinity of 27 micromolar, as well as the paradoxical Ca2+ influx associated with...</description>
            <author>Molecular Brain</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4219520</comments>
            <pubDate>Wed, 01 Dec 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4219520</guid>        </item>
        <item>
            <title>NMDAR2B tyrosine phosphorylation regulates anxiety-like behavior and CRF expression in the amygdala</title>
            <link>http://www.medworm.com/index.php?rid=4213576&amp;cid=s_37189_168_f&amp;fid=37189&amp;url=http%3A%2F%2Fwww.molecularbrain.com%2Fcontent%2F3%2F1%2F37</link>
            <description>Conclusions:
These data suggest that Tyr-1472 phosphorylation on GluN2B is important for anxiety-like behavior by negative regulation of CRF expression in the amygdala. (Source: Molecular Brain)</description>
            <author>Molecular Brain</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4213576</comments>
            <pubDate>Tue, 30 Nov 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4213576</guid>        </item>
        <item>
            <title>MATH5 controls the acquisition of multiple retinal cell fates</title>
            <link>http://www.medworm.com/index.php?rid=4179078&amp;cid=s_37189_168_f&amp;fid=37189&amp;url=http%3A%2F%2Fwww.molecularbrain.com%2Fcontent%2F3%2F1%2F36</link>
            <description>Math5-null mutation results in the loss of retinal ganglion cells (RGCs) and in a concurrent increase of amacrine and cone cells. However, it remains unclear whether there is a cell fate switch of Math5-lineage cells in the absence of Math5 and whether MATH5 cell-autonomously regulates the differentiation of the above retinal neurons. Here, we performed a lineage analysis of Math5-expressing cells in developing mouse retinas using a conditional GFP reporter (Z/EG) activated by a Math5-Cre knock-in allele. We show that during normal retinogenesis, Math5-lineage cells mostly develop into RGCs, horizontal cells, cone photoreceptors, rod photoreceptors, and amacrine cells. Interestingly, amacrine cells of Math5-lineage cells are predominately of GABAergic, cholinergic, and A2 subtypes, indicat...</description>
            <author>Molecular Brain</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4179078</comments>
            <pubDate>Thu, 18 Nov 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4179078</guid>        </item>
        <item>
            <title>Nigrostriatal neuronal death following chronic dichlorvos exposure: crosstalk between mitochondrial impairments, alpha synuclein aggregation, oxidative damage and behavioral changes.</title>
            <link>http://www.medworm.com/index.php?rid=4162761&amp;cid=s_37189_168_f&amp;fid=37189&amp;url=http%3A%2F%2Fwww.molecularbrain.com%2Fcontent%2F3%2F1%2F35</link>
            <description>Conclusion:
All these findings taken together indicate that chronic dichlorvos exposure may cause nigrostaital neurodegenaration and significant behavioral impairments. (Source: Molecular Brain)</description>
            <author>Molecular Brain</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4162761</comments>
            <pubDate>Sat, 13 Nov 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4162761</guid>        </item>
        <item>
            <title>Sex- and brain region-specific acceleration of beta-amyloidogenesis following behavioral stress in a mouse model of Alzheimer's disease</title>
            <link>http://www.medworm.com/index.php?rid=4151309&amp;cid=s_37189_168_f&amp;fid=37189&amp;url=http%3A%2F%2Fwww.molecularbrain.com%2Fcontent%2F3%2F1%2F34</link>
            <description>Conclusions:
Our results suggest that the higher prevalence of sporadic AD in women may be attributable to the vulnerability of female brains (especially, the hippocampus) to stressful events, which alter APP processing to favor the beta-amyloidogenesis through the transcriptional and translational upregulation of BACE1 combined with elevations in its substrate APP. (Source: Molecular Brain)</description>
            <author>Molecular Brain</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4151309</comments>
            <pubDate>Mon, 08 Nov 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4151309</guid>        </item>
        <item>
            <title>Lack of interleukin-1 type 1 receptor enhances the accumulation of mutant huntingtin in the
striatum and exacerbates the neurological phenotypes of Huntington's disease mice</title>
            <link>http://www.medworm.com/index.php?rid=4133285&amp;cid=s_37189_168_f&amp;fid=37189&amp;url=http%3A%2F%2Fwww.molecularbrain.com%2Fcontent%2F3%2F1%2F33</link>
            <description>Huntington's disease results from expansion of a glutamine repeat (&gt;36 glutamines) in the N-terminal region of huntingtin (htt) and is characterized by preferential neurodegeneration in the striatum of the brain. N171-82Q mice that express N-terminal 171 amino acids of htt with an 82-glutamine repeat show severe neurological phenotypes and die early, suggesting that N-terminal mutant htt is pathogenic. In addition, various cellular factors and genetic modifiers are found to modulate the cytotoxicity of mutant htt. Understanding the contribution of these factors to HD pathogenesis will help identify therapeutics for this disease. To investigate the role of interleukin type 1 (IL-1), a cytokine that has been implicated in various neurological diseases, in HD neurological symptoms, we crossed...</description>
            <author>Molecular Brain</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4133285</comments>
            <pubDate>Tue, 02 Nov 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4133285</guid>        </item>
        <item>
            <title>Altered synaptic plasticity in the mossy fibre pathway of transgenic mice expressing mutant amyloid precursor protein</title>
            <link>http://www.medworm.com/index.php?rid=4124686&amp;cid=s_37189_168_f&amp;fid=37189&amp;url=http%3A%2F%2Fwww.molecularbrain.com%2Fcontent%2F3%2F1%2F32</link>
            <description>Abeta peptides derived from the cleavage of amyloid precursor protein are widely believed to play an important role in the pathophysiology of Alzheimer's disease. A common way to study the impact these molecules on CNS function is to compare the physiology of transgenic mice that overproduce Abeta with non-transgenic animals. In the hippocampus, this approach has been frequently applied to investigation of synaptic transmission and plasticity in the perforant and Schaffer collateral commissural pathways, the first and third components of the classical hippocampal trisynaptic circuit, respectively. Similar studies however have not been carried out on the remaining component of the trisynaptic circuit, the mossy fibre pathway. Using transverse hippocampal slices prepared from ~2 year old ani...</description>
            <author>Molecular Brain</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4124686</comments>
            <pubDate>Mon, 01 Nov 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4124686</guid>        </item>
        <item>
            <title>M1 muscarinic receptor for the development of auditory cortical function</title>
            <link>http://www.medworm.com/index.php?rid=4097290&amp;cid=s_37189_168_f&amp;fid=37189&amp;url=http%3A%2F%2Fwww.molecularbrain.com%2Fcontent%2F3%2F1%2F29</link>
            <description>The sensory cortex is subject to continuous remodelling during early development and throughout adulthood. This process is important for establishing normal brain function and is dependent on cholinergic modulation via muscarinic receptors. Five muscarinic receptor genes encode five unique receptor subtypes (M1-5). The distributions and functions of each subtype vary in central and peripheral systems. In the brain, the M1 receptor is most abundant in the cerebral cortex, where its immunoreactivity peaks transiently during early development. This likely signifies the importance of M1 receptor in the development and maintenance of normal cortical function. Several lines of study have outlined the roles of M1 receptors in the development and plasticity of the auditory cortex. For example, M1-...</description>
            <author>Molecular Brain</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4097290</comments>
            <pubDate>Thu, 21 Oct 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4097290</guid>        </item>
        <item>
            <title>Molecular mechanisms of tiling and self-avoidance in neural development</title>
            <link>http://www.medworm.com/index.php?rid=4055617&amp;cid=s_37189_168_f&amp;fid=37189&amp;url=http%3A%2F%2Fwww.molecularbrain.com%2Fcontent%2F3%2F1%2F28</link>
            <description>Recent studies have begun to unravel the molecular basis of tiling and self-avoidance, two important cellular mechanisms that shape neuronal circuitry during development in both invertebrates and vertebrates. Dscams and Turtle (Tutl), two Ig superfamily proteins, have been shown to mediate contact-dependent homotypic interactions in tiling and self-avoidance. By contrast, the Activin pathway regulates axonal tiling in a contact-independent manner. These cell surface signals may directly or indirectly regulate the activity of the Tricornered kinase pathway and/or other intracellular signaling pathways to prevent the overlap between same-type neuronal arbors in the sensory or synaptic input field. (Source: Molecular Brain)</description>
            <author>Molecular Brain</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4055617</comments>
            <pubDate>Sun, 10 Oct 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4055617</guid>        </item>
        <item>
            <title>Calcium/calmodulin-dependent kinase IV contributes to translation-dependent early synaptic potentiation in the anterior cingulate cortex of adult mice</title>
            <link>http://www.medworm.com/index.php?rid=3976351&amp;cid=s_37189_168_f&amp;fid=37189&amp;url=http%3A%2F%2Fwww.molecularbrain.com%2Fcontent%2F3%2F1%2F27</link>
            <description>Calcium-calmodulin-dependent kinase IV (CaMKIV) phosphorylates the major transcription factor, cyclic AMP-responsive element binding protein (CREB), which plays key roles in synaptic plasticity and memory consolidation. Our previous study showed that long-term potentiation (LTP) in the anterior cingulate cortex (ACC) was significantly enhanced in transgenic mice overexpressing CaMKIV. Considering that the CaMKIV-CREB pathway plays a central role in the protein synthesis-dependent LTP, it is possible that upregulation of CaMKIV contributes to enhancement of LTP by promoting protein synthesis. To test this possibility, we examined the effects of transcription and translation inhibitors on synaptic potentiation induced by pairing of synaptic activity with postsynaptic depolarization (paired t...</description>
            <author>Molecular Brain</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3976351</comments>
            <pubDate>Wed, 15 Sep 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3976351</guid>        </item>
        <item>
            <title>The participation of NMDA receptors, PKC, and MAPK in the formation of memory following operant conditioning in Lymnaea</title>
            <link>http://www.medworm.com/index.php?rid=3920587&amp;cid=s_37189_168_f&amp;fid=37189&amp;url=http%3A%2F%2Fwww.molecularbrain.com%2Fcontent%2F3%2F1%2F24</link>
            <description>Conclusions:
The injection of either U0126 or GF109203X, which inhibit MAPK and PKC activity respectively, 1 hour prior to training results in the inhibition of both ITM and LTM formation. We further found that NMDA receptor activity was necessary in order for both ITM and LTM formation. (Source: Molecular Brain)</description>
            <author>Molecular Brain</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3920587</comments>
            <pubDate>Mon, 30 Aug 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3920587</guid>        </item>
        <item>
            <title>Roles of KChIP1 in the regulation of GABA-mediated transmission and behavioral anxiety</title>
            <link>http://www.medworm.com/index.php?rid=3812613&amp;cid=s_37189_168_f&amp;fid=37189&amp;url=http%3A%2F%2Fwww.molecularbrain.com%2Fcontent%2F3%2F1%2F23</link>
            <description>We report that KChIP1 is predominantly expressed at GABAergic synapses of a subset of parvalbumin-positive neurons in the brain. Forced expression of KChIP1 in cultured hippocampal neurons increased the frequency of miniature inhibitory postsynaptic currents (mIPSCs), reduced paired pulse facilitation of autaptic IPSCs, and decreases potassium current density. Furthermore, genetic ablation of KChIP1 potentiated potassium current density in neurons and caused a robust enhancement of anxiety-like behavior in mice. Our study suggests that KChIP1 is a synaptic protein that regulates behavioral anxiety by modulating inhibitory synaptic transmission, and drugs that act on KChIP1 may help to treat patients with mood disorders including anxiety. (Source: Molecular Brain)</description>
            <author>Molecular Brain</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3812613</comments>
            <pubDate>Sun, 01 Aug 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3812613</guid>        </item>
        <item>
            <title>A study of long-term potentiation in transgenic mice over-expressing mutant forms of both amyloid precursor protein and presenilin-1</title>
            <link>http://www.medworm.com/index.php?rid=3753609&amp;cid=s_37189_168_f&amp;fid=37189&amp;url=http%3A%2F%2Fwww.molecularbrain.com%2Fcontent%2F3%2F1%2F21</link>
            <description>Synaptic transmission and long-term potentiation (LTP) in the CA1 region of hippocampal slices have been studied during ageing of a double transgenic mouse strain relevant to early-onset familial Alzheimer's disease (AD). This strain, which over-expresses both the 695 amino acid isoform of human amyloid precursor protein (APP) with K670N and M671L mutations and presenilin 1 with the A246E mutation, has accelerated amyloidosis and plaque formation. There was a decrease in synaptic transmission in both wildtype and transgenic mice between 2 and 9 months of age. However, preparing slices from 14 month old animals in kynurenic acid (1 mM) counteracted this age-related deficit. Basal transmission and paired-pulse facilitation were similar between the two groups at all ages (2, 6, 9 and 14 month...</description>
            <author>Molecular Brain</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3753609</comments>
            <pubDate>Tue, 13 Jul 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3753609</guid>        </item>
        <item>
            <title>Dopamine D1 receptor-mediated NMDA receptor insertion depends on Fyn but not Src kinase pathway in prefrontal cortical neurons</title>
            <link>http://www.medworm.com/index.php?rid=3686953&amp;cid=s_37189_168_f&amp;fid=37189&amp;url=http%3A%2F%2Fwww.molecularbrain.com%2Fcontent%2F3%2F1%2F20</link>
            <description>Conclusions:
Dopamine D1 receptor-mediated increase of NMDA receptors is thus Fyn kinase dependent. Targeting this signaling pathway may be useful in treating drug addiction and schizophrenia. (Source: Molecular Brain)</description>
            <author>Molecular Brain</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3686953</comments>
            <pubDate>Mon, 21 Jun 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3686953</guid>        </item>
        <item>
            <title>Rab-mediated vesicular transport is required for neuronal positioning in the developing Drosophila visual system</title>
            <link>http://www.medworm.com/index.php?rid=3652193&amp;cid=s_37189_168_f&amp;fid=37189&amp;url=http%3A%2F%2Fwww.molecularbrain.com%2Fcontent%2F3%2F1%2F19</link>
            <description>Conclusions:
We propose that Rab5, Shi and Rab11 function together in a vesicular transport pathway for regulating R-cell positioning in the developing eye. (Source: Molecular Brain)</description>
            <author>Molecular Brain</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3652193</comments>
            <pubDate>Thu, 10 Jun 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3652193</guid>        </item>
        <item>
            <title>Emotional enhancement of memory: how norepinephrine enables synaptic plasticity</title>
            <link>http://www.medworm.com/index.php?rid=3563770&amp;cid=s_37189_168_f&amp;fid=37189&amp;url=http%3A%2F%2Fwww.molecularbrain.com%2Fcontent%2F3%2F1%2F15</link>
            <description>Changes in synaptic strength are believed to underlie learning and memory. We explore the idea that norepinephrine is an essential modulator of memory through its ability to regulate synaptic mechanisms. Emotional arousal leads to activation of the locus coeruleus with the subsequent release of norepineprine in the brain, resulting in the enhancement of memory. Norepinephrine activates both pre- and post-synaptic adrenergic receptors at central synapses with different functional outcomes, depending on the expression pattern of these receptors in specific neural circuitries underlying distinct behavioral processes. We review the evidence for noradrenergic modulation of synaptic plasticity with consideration of how this may contribute to the mechanisms of learning and memory. (Source: Molecu...</description>
            <author>Molecular Brain</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3563770</comments>
            <pubDate>Wed, 12 May 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3563770</guid>        </item>
        <item>
            <title>Iron content of ferritin modulates its uptake by intestinal epithelium: implications for co-transport of prions</title>
            <link>http://www.medworm.com/index.php?rid=3515167&amp;cid=s_37189_168_f&amp;fid=37189&amp;url=http%3A%2F%2Fwww.molecularbrain.com%2Fcontent%2F3%2F1%2F14</link>
            <description>In this report, we demonstrate that PrPSc and ferritin from CWD affected deer and elk brains and scrapie infected sheep resist degradation by digestive enzymes, and are transcytosed across a tight monolayer of human epithelial cells with significant efficiency. Likewise, ferritin from hamster brains is taken up by mouse intestinal epithelial cells in vivo, indicating that uptake of ferritin is not limited by species differences as described for prions. More importantly, the iron content of ferritin determines its efficiency of uptake and transport by Caco-2 cells and mouse models, providing insight into the mechanism(s) of ferritin and PrPSc uptake by intestinal epithelial cells. (Source: Molecular Brain)</description>
            <author>Molecular Brain</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3515167</comments>
            <pubDate>Wed, 28 Apr 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3515167</guid>        </item>
        <item>
            <title>LTP induction within a narrow critical period of immature stages enhances the survival of newly generated neurons in the adult rat dentate gyrus</title>
            <link>http://www.medworm.com/index.php?rid=3511408&amp;cid=s_37189_168_f&amp;fid=37189&amp;url=http%3A%2F%2Fwww.molecularbrain.com%2Fcontent%2F3%2F1%2F13</link>
            <description>In this study, we addressed whether a time period exists during which the survival of new neurons is maximally sensitive to the HFS. We found that the enhancement of cell survival by HFS was exclusively restricted to the specific narrow period during immature stages of new neurons (7-10 days after birth). Furthermore, the pharmacological blockade of LTP induction suppressed the enhancement of cell survival by the HFS. These results suggest that the LTP induction within a narrow critical period of immature stages enhances the survival of newly generated neurons in rat DG. (Source: Molecular Brain)</description>
            <author>Molecular Brain</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3511408</comments>
            <pubDate>Tue, 27 Apr 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3511408</guid>        </item>
        <item>
            <title>Rapid and Direct Transport of Cell Surface APP to the Lysosome defines a novel selective pathway</title>
            <link>http://www.medworm.com/index.php?rid=3490456&amp;cid=s_37189_168_f&amp;fid=37189&amp;url=http%3A%2F%2Fwww.molecularbrain.com%2Fcontent%2F3%2F1%2F11</link>
            <description>Conclusions:
These results demonstrate the presence of a novel, rapid and specific transport pathway from the cell surface to the lysosomes. This suggests that regulation of lysosomal traffic could regulate APP processing and that the lysosome could play a central role in the pathophysiology of Alzheimer's disease (Source: Molecular Brain)</description>
            <author>Molecular Brain</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3490456</comments>
            <pubDate>Tue, 20 Apr 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3490456</guid>        </item>
        <item>
            <title>Astrocytic expression of Parkinson's disease-related A53T alpha-synuclein causes neurodegeneration in mice</title>
            <link>http://www.medworm.com/index.php?rid=3490455&amp;cid=s_37189_168_f&amp;fid=37189&amp;url=http%3A%2F%2Fwww.molecularbrain.com%2Fcontent%2F3%2F1%2F12</link>
            <description>Conclusions:
Our findings demonstrate a critical involvement of astrocytic alpha-synuclein in initiating the non-cell autonomous killing of neurons, suggesting the viability of reactive astrocytes and microglia as potential therapeutic targets for PD and other neurodegenerative diseases. (Source: Molecular Brain)</description>
            <author>Molecular Brain</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3490455</comments>
            <pubDate>Tue, 20 Apr 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3490455</guid>        </item>
        <item>
            <title>Inhibition of AMPA receptor trafficking at hippocampal synapses by beta-amyloid oligomers: the mitochondrial contribution</title>
            <link>http://www.medworm.com/index.php?rid=3408146&amp;cid=s_37189_168_f&amp;fid=37189&amp;url=http%3A%2F%2Fwww.molecularbrain.com%2Fcontent%2F3%2F1%2F10</link>
            <description>Conclusions:
Our findings indicate that mitochondrial association with dendritic spines may play an important role in supporting AMPAR presence on or trafficking to the postsynaptic membrane. Abeta disruption of mitochondrial trafficking could contribute to AMPAR removal and trafficking defects leading to synaptic inhibition. (Source: Molecular Brain)</description>
            <author>Molecular Brain</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3408146</comments>
            <pubDate>Fri, 26 Mar 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3408146</guid>        </item>
        <item>
            <title>A quantitative proteomic analysis of long-term memory</title>
            <link>http://www.medworm.com/index.php?rid=3398733&amp;cid=s_37189_168_f&amp;fid=37189&amp;url=http%3A%2F%2Fwww.molecularbrain.com%2Fcontent%2F3%2F1%2F9</link>
            <description>Conclusions:
These results both confirm the involvement of previously identified memory proteins such as: protein kinase C (PKC), adenylate cyclase (AC), and proteins in the mitogen-activated protein kinase (MAPK) pathway. In addition these results provide novel protein candidates (e.g. UHRF1 binding protein) on which to base future studies. (Source: Molecular Brain)</description>
            <author>Molecular Brain</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3398733</comments>
            <pubDate>Tue, 23 Mar 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3398733</guid>        </item>
        <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 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>
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            <pubDate>Wed, 10 Sep 2008 04:00:00 +0100</pubDate>
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            <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>
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            <pubDate>Thu, 21 Aug 2008 04:00:00 +0100</pubDate>
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            <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>
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            <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>
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            <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>
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            <pubDate>Tue, 17 Jun 2008 04:00:00 +0100</pubDate>
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