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dl ‐Fenfluramine inhibits ethanol‐induced ascorbic acid release in rat striatum studied by microdialysis
Author(s) -
CHUNFU WU,
WEN LIU,
JING LIU,
CHYONHWA YEH
Publication year - 1998
Publication title -
addiction biology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.445
H-Index - 78
eISSN - 1369-1600
pISSN - 1355-6215
DOI - 10.1080/13556219872100
Subject(s) - microdialysis , chemistry , fenfluramine , ethanol , serotonergic , pharmacology , ascorbic acid , striatum , anorectic , medicine , endocrinology , serotonin , biochemistry , dopamine , receptor , body weight , food science , extracellular
The effects of dl ‐fenfluramine, dl ‐5‐hydroxytryptophan(5‐HTP) and fluoxetine on ethanol‐induced striatal ascorbic acid (AA) release in rat were studied by microdialysis coupled to high performance liquid chromatography with electrochemical detection. Ethanol (3.0 g/kg, i.p.) stimulated striatal AA release to more than 200% above the baseline. dl ‐Fenfluramine (20 mg/kg, i.p. or 40 mug/rat, i.c.v.), 10 min before ethanol administration, markedly inhibited ethanol‐induced AA release. A similar result was also observed following dl ‐5‐HTP (100 mg/kg, i.p.) administration. However, fluoxetine (10, 30 mg/kg, i.p.) showed no antagonistic effect on ethanol‐induced AA release. The suppressing effect of dl ‐fenfluramine and dl ‐5‐HTP on ethanolinduced AA release could be reversed by the 5‐HT receptor antagonist cyproheptadine (10 mg/kg, s.c.). All these drugs had no effect on basal AA release. The results give a first evidence for the involvement of central serotonergic system, and suggest that differential activities may exist between dl ‐fenfluramine, dl ‐5‐HTP and fluoxetine in regulating ethanol‐induced AA release in rat striatum.