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The endocannabinoid release is triggered by postsynaptic activation of voltage\u2010gated Ca<jats:sup>2+<\/jats:sup> channels and\/or G<jats:sub>q<\/jats:sub>\u2010coupled receptors such as group I metabotropic glutamate receptors (I\u2010mGluRs) and M<jats:sub>1<\/jats:sub>\/M<jats:sub>3<\/jats:sub> muscarinic receptors. However, the roles of NMDA receptors, which provide another pathway for Ca<jats:sup>2+<\/jats:sup> entry into neurons, in endocannabinoid signalling have been poorly understood. In the present study, we investigated the possible contribution of NMDA receptors in endocannabinoid production by recording IPSCs in cultured hippocampal neurons. Under the conditions minimizing the activation of voltage\u2010gated Ca<jats:sup>2+<\/jats:sup> channels, local application of NMDA (200 \u03bc<jats:sc>m<\/jats:sc>) transiently suppressed cannabinoid\u2010sensitive IPSCs, but not cannabinoid\u2010insensitive IPSCs. This NMDA\u2010induced suppression was abolished by blocking NMDA receptors, CB<jats:sub>1<\/jats:sub> receptors and diacylglycerol lipase, but not by inhibiting voltage\u2010gated Ca<jats:sup>2+<\/jats:sup> channels. When the postsynaptic neuron was dialysed with 30 m<jats:sc>m<\/jats:sc> BAPTA, the NMDA\u2010induced suppression was reduced significantly. A lower dose of NMDA (20 \u03bc<jats:sc>m<\/jats:sc>) exerted little effect when applied alone, but markedly enhanced the cannabinoid\u2010dependent suppression driven by muscarinic receptors or I\u2010mGluRs. These data clearly indicate that the activation of NMDA receptors facilitates the endocannabinoid release either alone or in concert with the G<jats:sub>q<\/jats:sub>\u2010coupled receptors.<\/jats:p>","DOI":"10.1113\/jphysiol.2007.137505","type":"journal-article","created":{"date-parts":[[2007,7,6]],"date-time":"2007-07-06T01:18:59Z","timestamp":1183684739000},"page":"407-418","source":"Crossref","is-referenced-by-count":56,"title":["Endocannabinoid signalling triggered by NMDA receptor\u2010mediated calcium entry into rat hippocampal 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