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    <title>Metaplastic control of the endocannabinoid system at inhibitory synapses in hippocampus.</title>
    <link>http://rss.neurobiologyoflipids.org/~r/lipoproteinsynapse/~3/322198177/query.fcgi</link>
    <description>&lt;table border="0" width="100%"&gt;&lt;tr&gt;&lt;td align="left"&gt;&lt;a href="http://www.pnas.org/cgi/pmidlookup?view=long&amp;amp;pmid=18523004"&gt;&lt;img src="http://www.ncbi.nlm.nih.gov/entrez/query/egifs/http:--highwire.stanford.edu-icons-externalservices-pubmed-custom-pnas_full.gif" border="0"/&gt;&lt;/a&gt; &lt;a href="http://hwmaint.pnas.org/cgi/pmidlookup?view=long&amp;amp;pmid=18523004"&gt;&lt;img src="http://www.ncbi.nlm.nih.gov/entrez/query/egifs/http:--highwire.stanford.edu-icons-externalservices-pubmed-custom-pnas_full_free.gif" border="0"/&gt;&lt;/a&gt; &lt;a href="http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pubmed&amp;amp;pubmedid=18523004"&gt;&lt;img src="http://www.ncbi.nlm.nih.gov/entrez/query/egifs/http:--www.pubmedcentral.nih.gov-corehtml-pmc-pmcgifs-pubmed-pmc.gif" border="0"/&gt;&lt;/a&gt; &lt;/td&gt;&lt;td align="right"&gt;&lt;a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed&amp;amp;cmd=Display&amp;amp;dopt=PubMed_PubMed&amp;amp;from_uid=18523004"&gt;Related Articles&lt;/a&gt;&lt;/td&gt;&lt;/tr&gt;&lt;/table&gt;
        &lt;p&gt;&lt;b&gt;Metaplastic control of the endocannabinoid system at inhibitory synapses in hippocampus.&lt;/b&gt;&lt;/p&gt;
        &lt;p&gt;Proc Natl Acad Sci U S A. 2008 Jun 10;105(23):8142-7&lt;/p&gt;
        &lt;p&gt;Authors:  Edwards DA, Zhang L, Alger BE&lt;/p&gt;
        &lt;p&gt;The modifiability of neuronal response plasticity is called "metaplasticity." In suppressing synaptic inhibition and facilitating induction of long-term excitatory synaptic plasticity, endocannabinoids (eCBs) act as agents of metaplasticity. We now report the discovery of a calcium-dependent mechanism that regulates eCB mobilization by metabotropic glutamate receptor (mGluR) activation. The switch-like mechanism primes cells to release eCBs and requires a transient rise in intracellular Ca2+ concentration ([Ca2+]i) but not concurrent activation of mGluRs. Conversely, short-term, [Ca2+]i-dependent eCB release can be persistently enhanced by mGluR activation. Hence, eCBs are also objects of metaplasticity, subject to higher levels of physiological control.&lt;/p&gt;
        &lt;p&gt;PMID: 18523004 [PubMed - indexed for MEDLINE]&lt;/p&gt;&lt;img src="http://rss.neurobiologyoflipids.org/~r/lipoproteinsynapse/~4/322198177" height="1" width="1"/&gt;</description>
    <author> Edwards DA, Zhang L, Alger BE</author>
    <category>Proc Natl Acad Sci U S A</category>
    <guid isPermaLink="false">PubMed:18523004</guid>
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