Biphasic effect of 5-methoxy-N,N-dimethyltryptamine on rat prolactin secretion.
Miljana Simonovic, Herbert Y. Meltzer
Brain Research August 8, 1983 DOI: 10.1016/0006-8993(83)90573-5 (opens in new tab)
Study at a glance
AI-extracted from the abstract| Characteristics | Experimental study Peer reviewed |
|---|---|
| Population | Rats |
| Interventions | 5-MeODMT 5-methoxytryptamine alpha-methylparatyrosine haloperidol gamma-butyrolactone quipazine |
| Dose | 2.5-10 mg/kg, 1-15 mg/kg, 10 mg/kg, 50 mg/kg, 0.15 mg/kg, 1 mg/kg, 500 mg/kg |
| Topics | 5-MeO-DMT DMT |
| Citations | 12 |
| Key findings | 5-MeODMT exerts a biphasic effect on rat prolactin secretion: initial short-term stimulation followed by inhibition of stimulated release, likely mediated by serotonin and dopamine pathways respectively. |
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.