Lysergic acid diethylamide: Evidence for stimulation of pituitary dopamine receptors
Herbert Y. Meltzer, Richard G. Fessler, Miljana Simonovic, John Doherty, Victor S. Fang
Psychopharmacology January 1, 1977 DOI: 10.1007/bf00426539 via Springer Nature
Summary
Lysergic acid diethylamide (LSD) at doses of 0.05 mg/kg and 0.20 mg/kg significantly lowered plasma prolactin levels in male rats. The higher dose also blocked prolactin increases caused by chlorpromazine and alpha-methylparatyrosine, drugs that reduce dopaminergic inhibition of prolactin secretion. LSD was more potent than methysergide, a serotonin blocker, in lowering prolactin, and more potent than apomorphine, a dopamine agonist, in blocking prolactin rises from quipazine, a serotonin agonist. These results suggest LSD acts as a potent dopamine agonist on pituitary or hypothalamic receptors that inhibit prolactin secretion.
Study at a glance
| Characteristics | Experimental study Peer reviewed |
|---|---|
| Population | Male rats |
| Topics | LSD Serotonin |
| Keywords | Prolactin Dopamine Methysergide |
| Key finding | LSD has potent dopamine agonist properties that directly or indirectly inhibit prolactin secretion in male rats. |
Abstract
Lysergic acid diethylamide (LSD), 0.05 mg/kg and 0.20 mg/kg, significantly decreased plasma prolactin (PRL) levels in male rats. LSD, 0.20 mg/kg, also inhibits the increase in plasma PRL levels produced by chlorpromazine (CPZ), 5 mg/kg, and alpha-methylparatyrosine (AMPT), 50 mg/kg, both of which interfere with dopaminergic inhibition of PRL secretion. LSD was more potent than methysergide, a serotonin receptor blocker, in lowering plasma PRL levels and more potent than apomorphine, a known direct acting dopamine agonist, in blocking the increase in plasma PRL produced by quipazine, a 5-HT agonist. These results suggest LSD has potent dopamine agonist properties on the rat pituitary or hypothalamic dopamine receptors which directly or indirectly inhibit PRL secretion.