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Besides the well\u2010known adverse effects of cardiovascular and respiratory depression, recent studies indicate that propofol may cause excitatory phenomena such as myoclonus, opisthotonus, and even seizure. However, the mechanisms of these excitatory effects of propofol have not been elucidated. Considering glutamate as the principle excitatory neurotransmitter in the central nervous system and excessive glutamatergic synaptic transmission can cause seizure, we examined the effect of propofol on the release of glutamate from rat cerebral cortex nerve terminals (synaptosomes). Results showed that subanesthetic concentration propofol facilitated 4\u2010aminopyridine (4\u2010AP), but not KCl\u2010 or ionomycin\u2010evoked glutamate release from nerve terminals. The facilitation of 4\u2010AP\u2010evoked glutamate release by propofol also occurred in the calcium chelation and significantly attenuated by glutamate transporter inhibitors, <jats:sc>DL<\/jats:sc>\u2010threo\u2010\u03b2\u2010benzyloxyaspartic acid (<jats:sc>DL<\/jats:sc>\u2010TBOA) and <jats:sc>L<\/jats:sc>\u2010<jats:italic>trans<\/jats:italic>\u2010pyrrolidine\u20102,4\u2010dicarboxylic acid (<jats:sc>L<\/jats:sc>\u2010<jats:italic>trans<\/jats:italic>\u2010PDC). In addition, propofol increased 4\u2010AP\u2010evoked depolarization of the plasma membrane potential. Furthermore, protein kinase C (PKC) inhibition suppressed propofol\u2010mediated facilitation of glutamate release. These results suggest that subanesthetic concentration propofol facilitates glutamate release from rat cerebrocortical glutamatergic terminals by increasing nerve terminal excitability, likely through the activation of PKC pathway. This finding may provide an explanation for propofol\u2010induced excitatory phenomena. Synapse 63:773\u2013781, 2009. \u00a9 2009 Wiley\u2010Liss, Inc.<\/jats:p>","DOI":"10.1002\/syn.20656","type":"journal-article","created":{"date-parts":[[2009,6,2]],"date-time":"2009-06-02T05:14:11Z","timestamp":1243919651000},"page":"773-781","source":"Crossref","is-referenced-by-count":17,"title":["Facilitation of glutamate release from rat cerebral cortex nerve terminal by subanesthetic concentration 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