{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,17]],"date-time":"2026-10-17T19:19:24Z","timestamp":1792264764985,"version":"4.4.0"},"reference-count":61,"publisher":"Wiley","issue":"13","license":[{"start":{"date-parts":[[2022,6,8]],"date-time":"2022-06-08T00:00:00Z","timestamp":1654646400000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":["physoc.onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["The Journal of Physiology"],"published-print":{"date-parts":[[2022,7]]},"abstract":"<jats:sec><jats:title>Abstract<\/jats:title><jats:p>Cholinergic neurones in the basal forebrain (BF) project into various brain regions and receive excitatory inputs from the cortex and brain stem. These cholinergic neurones receive serotonergic fibres from the dorsal raphe nuclei. This study was aimed to elucidate serotonin (5\u2010HT)\u2010induced modulation of glutamatergic transmission onto rat BF cholinergic neurones identified with Cy3\u2010192IgG. Excitatory postsynaptic currents (EPSCs) were evoked by focal stimulation. Bath application of either 5\u2010HT, the 5\u2010HT<jats:sub>1A<\/jats:sub> receptor agonist 8\u2010OH\u2010DPAT (DPAT), or the 5\u2010HT<jats:sub>1B<\/jats:sub> receptor agonist CP93129 (CP), inhibited the amplitude of EPSCs. In the presence of both 5\u2010HT<jats:sub>1A<\/jats:sub> and 5\u2010HT<jats:sub>1B<\/jats:sub> receptor antagonists, the 5\u2010HT\u2010induced effect disappeared. The paired\u2010pulse ratio (PPR) and coefficient of variation (CV) of the EPSCs were increased by CP, whereas DPAT had no effect on PPR or CV. DPAT inhibited the inward currents induced by puff application of <jats:sc>l<\/jats:sc>\u2010glutamate, which were unaffected by CP. DPAT suppressed the amplitude of miniature EPSCs (mEPSCs) without affecting their frequency. CP decreased the frequency of mEPSCs in more than half of the neurones examined, whereas the amplitude was unaffected. DPAT or CP alone inhibited the NMDA receptor\u2010mediated currents. 5\u2010HT\u2010induced inhibition of EPSCs was reduced in the presence of \u03c9\u2010agatoxin TK (Aga). Furthermore, CP\u2010induced inhibition of EPSCs was eliminated in the presence of Aga. DPAT\u2010induced inhibition of EPSCs was unchanged in the presence of Aga. These results suggest that activation of 5\u2010HT<jats:sub>1A<\/jats:sub> receptors reduces the sensitivity of postsynaptic glutamate receptors to glutamate, whereas presynaptic activation of 5\u2010HT<jats:sub>1B<\/jats:sub> receptors inhibits glutamate release by blocking P\/Q\u2010type calcium channels.\n<jats:boxed-text content-type=\"graphic\" position=\"anchor\"><jats:graphic xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" mimetype=\"image\/png\" position=\"anchor\" specific-use=\"enlarged-web-image\" xlink:href=\"graphic\/tjp15128-gra-0001-m.png\"><jats:alt-text>image<\/jats:alt-text><\/jats:graphic><\/jats:boxed-text><\/jats:p><\/jats:sec><jats:sec><jats:title>Key points<\/jats:title><jats:p><jats:list list-type=\"bullet\">\n<jats:list-item><jats:p>We performed a patch\u2010clamp study to investigate serotonin (5\u2010HT)\u2010induced modulation of glutamatergic transmission onto cholinergic neurones in the rat basal forebrain slices.<\/jats:p><\/jats:list-item>\n<jats:list-item><jats:p>Excitatory postsynaptic currents (EPSCs) were inhibited by 5\u2010HT as well as agonists of 5\u2010HT<jats:sub>1A<\/jats:sub> or 5\u2010HT<jats:sub>1B<\/jats:sub> receptors. 5\u2010HT\u2010induced inhibition was antagonized by co\u2010application of 5\u2010HT<jats:sub>1A<\/jats:sub> and 5\u2010HT<jats:sub>1B<\/jats:sub> receptor antagonists.<\/jats:p><\/jats:list-item>\n<jats:list-item><jats:p>The effects of 5\u2010HT receptor agonists on the paired\u2010pulse ratio, coefficient of variation of EPSCs, inward currents induced by puff application of <jats:sc>l<\/jats:sc>\u2010glutamate as well as miniature EPSCs suggest that activation of 5\u2010HT<jats:sub>1A<\/jats:sub> receptors decreases the sensitivity of postsynaptic glutamate receptors to glutamate, whereas 5\u2010HT<jats:sub>1B<\/jats:sub> receptors presynaptically inhibit glutamate release.<\/jats:p><\/jats:list-item>\n<jats:list-item><jats:p>The 5\u2010HT<jats:sub>1B<\/jats:sub> agonist\u2010induced inhibition was eliminated in the presence of a P\/Q\u2010type calcium channel blocker, whereas the 5\u2010HT<jats:sub>1A<\/jats:sub> agonist still inhibited the EPSCs even in the presence of the blocker.<\/jats:p><\/jats:list-item>\n<jats:list-item><jats:p>The present study reveals different pre\u2010 and postsynaptic mechanisms underlying 5\u2010HT<jats:sub>1A<\/jats:sub> and 5\u2010HT<jats:sub>1B<\/jats:sub> receptor\u2010mediated modulation of excitatory transmission.<\/jats:p><\/jats:list-item>\n<\/jats:list><\/jats:p><\/jats:sec>","DOI":"10.1113\/jp282509","type":"journal-article","created":{"date-parts":[[2022,5,22]],"date-time":"2022-05-22T15:25:04Z","timestamp":1653233104000},"page":"3149-3167","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":18,"title":["Serotonin 5\u2010HT<sub>1A<\/sub> and 5\u2010HT<sub>1B<\/sub> receptor\u2010mediated inhibition of glutamatergic 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