{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,4,18]],"date-time":"2026-04-18T11:43:13Z","timestamp":1776512593916,"version":"3.51.2"},"reference-count":45,"publisher":"American Association for the Advancement of Science (AAAS)","issue":"4194","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Science"],"published-print":{"date-parts":[[1975,6,20]]},"abstract":"<jats:p>Neuroleptic (antipsychotic) drugs inhibited the electrically stimulated release of [<jats:sup>3<\/jats:sup>H]dopamine from rat striatal slices. The concentrations for 50 percent inhibition (ranging from 11.5 nanomolar for spiroperidol to 800 nanomolar for thioridazine) correlated closely with the average daily dosages of 25 neuroleptic drugs used clinically for schizophrenia. The correlation includes butyrophenones, phenothiazines, reserpine, pimozide, clozapine, and (+)-butaclamol. Clinically inactive isomers [<jats:italic>trans<\/jats:italic>-thiothixene,<jats:italic>trans<\/jats:italic>-flupenthixol, and (-)-butaclamol] required 20 to 1000 times higher concentrations than the active isomers to inhibit release. Compared to the inhibition of [<jats:sup>3<\/jats:sup>H]dopamine release, much higher neuroleptic concentrations were needed to inhibit the electrically stimulated release of other neurotransmitters\u2014[<jats:sup>3<\/jats:sup>H]acetylcholine, [<jats:sup>3<\/jats:sup>H]GABA (\u03b3-aminobutyric acid). 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