Inhibition of prolactin release by stimulation of presynaptic serotonin autoreceptors.
Life Sciences December 6, 1982 DOI: 10.1016/0024-3205(82)90740-8 (opens in new tab) via PubMed
Summary
AI-generated from the abstractIn male rats, the serotonin agonist 5-MeODMT did not alter basal prolactin levels at doses from 1.0 to 20.0 mg/kg. However, pretreatment with 5-MeODMT reduced prolactin release stimulated by agents that rely on serotonergic neurotransmission, specifically L-5-hydroxytryptophan (5-HTP) and morphine. These results suggest that 5-MeODMT acts as a presynaptic serotonin autoreceptor stimulant rather than a post-synaptic serotonin agonist in the neuronal systems controlling prolactin release.
Study at a glance
| Characteristics | Experimental study Peer reviewed |
|---|---|
| Population | Male rats |
| Interventions | 5-methoxy-N N-dimethyltryptamine (5-MeODMT) |
| Dose | 1.0, 2.0, 5.0, 10.0, 20.0 mg/kg |
| Citations | 8 |
| Key finding | 5-MeODMT acts as a presynaptic serotonin autoreceptor stimulant, not a post-synaptic agonist, in the control of prolactin release. |
Abstract
The effects of 5-methoxy-N,N-dimethyltryptamine (5-MeODMT), a serotonin agonist with a preferential action on presynaptic autoreceptors, on prolactin release in male rats was determined. Basal serum prolactin levels were not altered after administration of 1.0, 2.0, 5.0, 10.0 or 20.0 mg/kg of 5-MeODMT. Pretreatment with 5-MeODMT reduced prolactin release by agents that depend on serotonergic neurotransmission for part of their prolactin release stimulation. Prolactin release in response to L-5-hydroxytryptophan (5-HTP) or morphine was significantly reduced by pretreatment of the rats with 5-MeODMT. The results of this experiment indicate that 5-MeODMT acts as a presynaptic serotonin autoreceptor stimulant and not as a post-synaptic serotonin agonist on the neuronal systems that control prolactin release.