Abstract
Intraperitoneal administration of phencyclidine (PCP, 2.5–20 mg/kg) produced a dose-related inhibition of the increase in serum PRL concentrations produced by α-methylparatyrosine (AMPT) or reserpine, but not morphine. Phencyclidine was more potent in antagonizing the PRL-releasing effect of reserpine than that of AMPT, suggesting a greater effect of PCP on the cytoplasmic than the storage dopamine (DA) pool. Phencyclidine had no effect on PRL release from rat pituitary glands in vitro. Intravenous administration of PCP (10 mg/kg) to anesthetized male rats produced a two-fold increase in pituitary stalk (DA) concentrations, suggesting that PCP inhibits rat serum PRL by increasing the release of DA from the tuberoinfundibular neurons, and possibly by blocking its reuptake as well.
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