Stimulation of rat prolactin secretion by indolealkylamine hallucinogens.
H Y Meltzer, R G Fessler, M Simonovic, V S Fang
Psychopharmacology April 11, 1978 DOI: 10.1007/BF00432847 via PubMed
Summary
AI-generated from the abstractSeveral hallucinogenic indoleamine drugs, including N,N-dimethyltryptamine (N,N-DMT), psilocybin, bufotenin, 5-methoxy-N,N-dimethyltryptamine, and N-methyltryptamine, increased levels of the hormone prolactin (PRL) in rat plasma. The effect of N,N-DMT, psilocybin, and bufotenin was blocked by methysergide, a serotonin receptor blocker. Inhibiting serotonin synthesis with parachlorophenylalanine (PCPA) made the PRL increase from N,N-DMT and psilocybin stronger. A toxin that selectively damages serotonin neurons also enhanced the PRL response to N,N-DMT. These results suggest the drugs stimulate PRL release by acting as serotonin agonists. Bufotenin, which poorly crosses the blood-brain barrier, had the strongest effect on PRL, hinting that the relevant serotonin receptors might be outside the barrier or that central receptors are especially sensitive to it.
Study at a glance
| Characteristics | Experimental study Peer reviewed |
|---|---|
| Population | Rats |
| Interventions | N N-dimethyltryptamine psilocybin bufotenin 5-methoxy-N N-methyltryptamine methysergide parachlorophenylalanine parachloroamphetamine |
| Citations | 24 |
| Key finding | Indole hallucinogens increase rat plasma prolactin levels through a serotonergic agonist mechanism, with bufotenin showing the most potent effect despite poor blood-brain barrier penetration. |
Abstract
The hallucinogenic indoleamine drugs N,N-dimethyltryptamine (N,N-DMT), psilocybin, bufotenin, 5-methoxy-N,N-dimethyltryptamine, and N-methyltryptamine, increased rat plasma prolactin (PRL) levels. The increase in plasma PRL produced by N,N-DMT, psilocybin, and bufotenin was inhibited by methysergide, a serotonin receptor blocker. Parachlorophenylalanine (PCPA), an inhibitor of serotonin synthesis, significantly potentiated the increase in PRL produced by N,N-DMT, and psilocybin. Parachloroamphetamine, a relatively selective toxin for serotonin neurons, also stimulated the increase in PRL produced by N,N-DMT. These results suggest that the indole hallucinogens stimulate PRL secretion by a serotonergic agonist mechanism. Bufotenin has been reported to pass the blood-brain barrier poorly, but of the indoles studied it had the most potent effect on PRL secretion. This raises the possibility that the serotonin receptors which promote PRL secretion may be outside the blood-brain barrier or that the central 5-HT receptors which mediate PRL secretion may be especially responsive to bufotenin.