Effect of midbrain raphe lesion or 5,7-dihydroxytryptamine treatment on the prolactin-releasing action of quipazine andd-fenfluramine in rats
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TL;DR
The results suggest that the effect of quipazine and D-fenfluramine on PRL release is mediated through a serotonergic mechanism in the brain.
Abstract
The role of brain serotonin in regulating prolactin (PRL) secretion has been investigated by studying the effect of quipazine and D-fenfluramine, two serotonin-like drugs, on plasma PRL levels under various experimental conditions. Quipazine (5, 10 and 20 mg/kg i.p.) and D-fenfluramine (5, 7.5 and 10 mg/kg i.p.) induced dose-related increases in plasma PRL levels in male rats. Intraventricular injection of 5,7-dihydroxytryptamine (5,7-DHT) or electrolytic lesion of the nucleus raphe medianus (MR), which caused a marked and selective depletion of hypothalamic serotonin levels, significantly reduced the PRL-releasing effect of both quipazine and D-fenfluramine. These results suggest that the effect of these drugs on PRL release is mediated through a serotonergic mechanism in the brain.
