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Meltzer HY, Fessler RG, Simonovic M, Doherty J, Fang VS. 
“Lysergic Acid Diethylamide: Evidence for Stimulation of Pituitary Dopamine Receptors”. 
Psychopharmacology. 1977;54(1):39-44.
The effects of LSD on prolactin (PRL) secretion in the rat - were investigated. Methods Male Sprague-Dawley rats (150-200 g) wre used. All drugs were dissolved in saline and injected i.p.. Rats were injected with ketamine 100 mg/kg i.p. prior to sacrifice. Heparinized blood was obtained from the inferior vena cave. Plasma samples were frozen and later assayed for PRL by a double antibody radio immunoassay. LSD (0.05 and 0.2 mg/kg) significantly decreased plasma PRL levels in male rats. Methysergide (Sandoz) (10 mg/kg), also significantly decreased rat plasma PRL levels. LSD (0.2 mg/kg and 0.5 mg/kg) significantly inhibited the increase in PRL produced by chlorpromazine (CPZ) (SK+F) (5 mg/kg i.p.). Apo morphine (Merck-USA) (0.5 mg/kg) significantly inhibited the effect of CPZ. The effect of LSD (0.2 mg/kg) on the PRL response to CPZ was significantly greater than that of the same dose of apomorphine. Both LSD (0.2 mg/kg) and apomorphine (5.0 mg/kg) significantly inhibited the increase In plasma PRL produced by a-methyl-p-tyrosine (Sigma-Chem.) (50 mg/kg). LSD (0.5 mg/kg) completely Inhibited the increase in plasma PRL produced by quipazine (Miles) (5 mg/kg), in naive rats or rats pretreated with p-chlorophenylalanine-methylester (PCPA) (Sigma-Chem.). Methysergide (5 mg/kg) also inhibited the increase in PRL produced by quipazine and PCPA plus quipazine. The lowering of plasma PRL in male rats by LSD is the result of dopamine agonist properties rather than 5-HT antagonist properties.
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