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IS RECEPTOR ACTIVATION INVOLVED IN THE MECHANISM BY WHICH (+)‐FENFLURAMINE AND (+)‐NORFENFLURAMINE DEPLETE 5‐HYDROXYTRYPTAMINE IN THE RAT BRAIN?
Author(s) -
INVERNIZZI R.,
KMIECIAKKOLADA K.,
SAMANIN R.
Publication year - 1982
Publication title -
british journal of pharmacology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.432
H-Index - 211
eISSN - 1476-5381
pISSN - 0007-1188
DOI - 10.1111/j.1476-5381.1982.tb09169.x
Subject(s) - fenfluramine , reserpine , chemistry , pharmacology , 5 ht receptor , brainstem , cerebrum , medicine , serotonin , endocrinology , receptor , central nervous system , biology , biochemistry
1 The effects of (+)‐fenfluramine, (+)‐norfenfluramine and reserpine on the concentrations of 5‐hydroxytryptamine (5‐HT) and 5‐hydroxyindoleacetic acid (5‐HIAA) in brainstem and telencephalon were studied in rats treated with methergoline, a 5‐HT antagonist. 2 Methergoline significantly reduced the effect of (+)‐norfenfluramine (5 mg/kg) on 5‐HT levels in telencephalon and brainstem but did not modify the effect of (+)‐norfenfluramine (2.5 mg/kg). 3 Neither the effect of (+)‐fenfluramine on 5‐HT levels nor the decrease of 5‐HT metabolism caused by (+)‐fenfluramine and (+)‐norfenfluramine was significantly modified by methergoline treatment. 4 Methergoline potentiated the effects of reserpine on brain indoles. The effect was particularly evident on 5‐HIAA levels in the brainstem, although significant effects were found on 5‐HT in the brainstem and 5‐HIAA in the telencephalon depending on the dose of reserpine used. 5 The results show that postsynaptic receptor activation may partially contribute to the depletion of brain 5‐HT caused by (+)‐norfenfluramine in the rat. This mechanism does not seem to play a significant role in the effect of (+)‐fenfluramine.