| Literature DB >> 140381 |
J B Malick, E Doren, A Barnett.
Abstract
Quipazine has been reported to be a direct serotonin receptor agonist. In this laboratory, quipazine produced head-twitch in mice similar to that produced by the serotonin precursor, 5-hydroxytryptophan (5-HTP). Three antiserotonergic drugs (methiothepin, methysergide, and cinanserin) antagonized both the 5-HTP and quipazine-induced head-twitch responses. In addition, the quipazine response was significantly potentiated by a monoamine oxidase (MAO) inhibitor, pargyline. Since it is not likely that quipazine itself is metabolized by MAO, these results suggested that quipazine might cause release of endogenous serotonin. Parachlorophenylalanine, a serotonin depletor, significantly antagonized the potentiation of quipazine by the MAO inhibitor but failed to antagonize the head-twitch produced by quipazine itself. The present studies suggest that quipazine influences serotonin receptors in the brain to produce head-twitch by two mechanisms of action: (1) by direct serotonin receptor activation, and (2) indirectly by causing a release of endogenous serotonin.Entities:
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Year: 1977 PMID: 140381 DOI: 10.1016/0091-3057(77)90032-6
Source DB: PubMed Journal: Pharmacol Biochem Behav ISSN: 0091-3057 Impact factor: 3.533