Biphasic effect of 5-methoxy-N,N-dimethyltryptamine on rat prolactin secretion.
Brain research – August 08, 1983
Source: PubMed
Summary
5-Methoxy-N,N-dimethyltryptamine (5-MeODMT) significantly impacts prolactin (PRL) secretion in rats, showing a dose-dependent initial increase at doses of 2.5-10 mg/kg, lasting under 30 minutes. With higher doses (1-15 mg/kg), it inhibits PRL stimulation from other serotonin agonists like 5-methoxytryptamine (5-MeOT). Notably, 5-MeODMT did not affect PRL release induced by gamma-butyrolactone or high-dose haloperidol. This biphasic response suggests that 5-MeODMT first activates serotonin receptors before enhancing dopamine neuron activity, influencing PRL regulation.
Abstract
5-Methoxy-N,N-dimethyltryptamine (5-MeODMT), a potent serotonin (5-HT) receptor agonist, exerts a biphasic effect on rat prolactin (PRL) secretion. 5-MeODMT (2.5-10 mg/kg) produces a marked, dose-related but short-lasting (less than 30 min) rise in serum PRL levels. At intervals longer than 30 min, 5-MeODMT (1-15 mg/kg) inhibits the stimulation of PRL secretion by another 5-HT agonist, 5-methoxytryptamine (5-MeOT, 10 mg/kg), by alpha-methylparatyrosine (50 mg/kg) or by haloperidol (0.15 mg/kg). 5-MeODMT did not significantly alter the PRL-releasing effect of gamma-butyrolactone (500 mg/kg) or a higher dose of haloperidol (1 mg/kg). The biphasic effect of 5-MeODMT on rat PRL secretion is shared by the centrally-acting 5-HT agonist quipazine, but not by 5-MeOT, an indole derivative excluded by the blood-brain barrier. The initial stimulation of PRL secretion by 5-MeODMT is probably due to its ability to activate postsynaptic 5-HT receptors. The subsequent inhibitory effect of 5-MeODMT appears to be due to increased functional activity of tuberoinfundibular dopamine neurons. The possible mechanisms underlying the inhibitory effect of 5-MeODMT on PRL release are discussed.