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GABAA<\/jats:sub><\/jats:styled-content> receptor\u2010mediated inhibitory postsynaptic currents (IPSC<\/jats:styled-content>s) were evoked by focal stimulation. Bath application of 5\u2010HT<\/jats:styled-content> (0.1\u2013300\u00a0\u03bcm<\/jats:sc>) reversibly suppressed the amplitude of evoked IPSC<\/jats:styled-content>s in a concentration\u2010dependent manner. Application of a 5\u2010HT<\/jats:styled-content>1B<\/jats:sub> receptor agonist, CP<\/jats:styled-content>93129, also suppressed the evoked IPSC<\/jats:styled-content>s, whereas a 5\u2010HT<\/jats:styled-content>1A<\/jats:sub> receptor agonist, 8\u2010OH<\/jats:styled-content>\u2010DPAT<\/jats:styled-content> had little effect on the evoked IPSC<\/jats:styled-content>s amplitude. In the presence of NAS<\/jats:styled-content>\u2010181, a 5\u2010HT<\/jats:styled-content>1B<\/jats:sub> receptor antagonist, 5\u2010HT<\/jats:styled-content>\u2010induced suppression of evoked IPSC<\/jats:styled-content>s was antagonised, whereas NAN<\/jats:styled-content>\u2010190, a 5\u2010HT<\/jats:styled-content>1A<\/jats:sub> receptor antagonist did not antagonise the 5\u2010HT<\/jats:styled-content>\u2010induced suppression of evoked IPSC<\/jats:styled-content>s. Bath application of 5\u2010HT<\/jats:styled-content> reduced the frequency of spontaneous miniature IPSC<\/jats:styled-content>s without changing their amplitude distribution. The effect of 5\u2010HT<\/jats:styled-content> on miniature IPSC<\/jats:styled-content>s remained unchanged when extracellular Ca2+<\/jats:sup> was replaced by Mg2+<\/jats:sup>. The paired\u2010pulse ratio was increased by CP<\/jats:styled-content>93129. In the presence of \u03c9\u2010CgTX<\/jats:styled-content>, the N\u2010type Ca2+<\/jats:sup> channel blocker, \u03c9\u2010Aga\u2010TK<\/jats:styled-content>, the P\/Q\u2010type Ca2+<\/jats:sup> channel blocker, or SNX<\/jats:styled-content>\u2010482, the R\u2010type Ca2+<\/jats:sup> channel blocker, 5\u2010HT<\/jats:styled-content> could still inhibit the evoked IPSC<\/jats:styled-content>s. 4\u2010AP<\/jats:styled-content>, a K+<\/jats:sup> channel blocker, enhanced the evoked IPSC<\/jats:styled-content>s, and CP<\/jats:styled-content>93129 had no longer inhibitory effect in the presence of 4\u2010AP<\/jats:styled-content>. CP<\/jats:styled-content>93129 increased the number of action potentials elicited by depolarising current pulses. These results suggest that activation of presynaptic 5\u2010HT<\/jats:styled-content>1B<\/jats:sub> receptors on the terminals of GABA<\/jats:styled-content>ergic afferents to basal forebrain cholinergic neurons inhibits GABA<\/jats:styled-content> release in Ca2+<\/jats:sup> influx\u2010independent manner by modulation of K+<\/jats:sup> channels, leading to enhancement of neuronal activities.<\/jats:p>","DOI":"10.1111\/ejn.13273","type":"journal-article","created":{"date-parts":[[2016,5,14]],"date-time":"2016-05-14T06:13:11Z","timestamp":1463206391000},"page":"1747-1760","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":18,"title":["Serotonin 5\u2010HT<\/scp>1B<\/sub> receptor\u2010mediated calcium influx\u2010independent presynaptic inhibition of GABA<\/scp> release onto rat basal forebrain cholinergic neurons"],"prefix":"10.1111","volume":"44","author":[{"given":"Takuma","family":"Nishijo","sequence":"first","affiliation":[{"name":"Department of Pharmacology Jikei University School of Medicine Nishi\u2010Shimbashi, Minato\u2010ku Tokyo 105\u20108461 Japan"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Toshihiko","family":"Momiyama","sequence":"additional","affiliation":[{"name":"Department of Pharmacology Jikei University School of Medicine Nishi\u2010Shimbashi, Minato\u2010ku Tokyo 105\u20108461 Japan"}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"311","published-online":{"date-parts":[[2016,6,4]]},"reference":[{"key":"e_1_2_9_2_1","doi-asserted-by":"publisher","DOI":"10.1113\/jphysiol.1986.sp016347"},{"key":"e_1_2_9_3_1","doi-asserted-by":"publisher","DOI":"10.1080\/15622970802465807"},{"key":"e_1_2_9_4_1","doi-asserted-by":"publisher","DOI":"10.1152\/jn.00543.2003"},{"key":"e_1_2_9_5_1","doi-asserted-by":"publisher","DOI":"10.1126\/science.1058803"},{"key":"e_1_2_9_6_1","doi-asserted-by":"publisher","DOI":"10.1016\/0014-2999(88)90799-6"},{"key":"e_1_2_9_7_1","doi-asserted-by":"publisher","DOI":"10.1371\/journal.pone.0148169"},{"key":"e_1_2_9_8_1","doi-asserted-by":"publisher","DOI":"10.1016\/0306-4522(95)00109-V"},{"key":"e_1_2_9_9_1","doi-asserted-by":"crossref","first-page":"3130","DOI":"10.1523\/JNEUROSCI.23-08-03130.2003","article-title":"Presynaptic modulation of the retinogeniculate synapse","volume":"23","author":"Chen C.","year":"2003","journal-title":"J. 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