Dopaminergic and Opioid Compounds

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Abstract
In ovariectomized rhesus monkeys (Macaco mulatto) electrical stimulation (ES) of the medial basal hypothalamus (MBH) for 30 min with stimulus parameters that caused no overt behavioral responses elicited 7-fold and 2-fold increases in serum concentrations of prolactin (Prl) and luteinizing hormone (LH), respectively, 15–30 min after the onset of ES. Intravenous infusion of dopamine (5, 10, or 40, µg/kg body weight/min) for 1 h beginning 30 min before ES markedly reduced (5- and 10-µg doses, p < 0.05) or inhibited (40-µg dose, p < 0.01) the electrically induced rise in serum Prl. Infusion of apomorphine, a drug that stimulates dopamine receptors, also suppressed or abolished the electrically induced elevation in serum Prl at doses of 100 and 150 µg/kg b.w./min, respectively. Neither drug affected the increase in serum LH levels that occurred after MBH-ES since the pattern of LH release was similar in saline-and drug-treated ES animals (p > 0.05). Moreover, the 40-µg of the endogenous opiate, β-endorphin, also elicited an increase in serum Prl to more than preinject¡on levels (p < 0.05). Infusion of naloxone · HCl (an opiate antagonist) at a dose of 10/fg/kg b.w./min for 50 min blocked the rise in serum Prl after the injection of β-endrophin. Naloxone infusion at 10 and 20 µg/kg/min for 1 h beginning 30 min before MBH-ES had no effect on Prl or LH release (p > 0.05). However, these same naloxone regimens markedly reduced the rise in serum Prl after ES of the lostral hypothalamus (p < 0.01). Thus, within the MBH-pituitary unit of the rhesus monkey, dopamine appears to play a role in the electrically induced release of Prl. but not of LH. Although β-endorphin can initiate release of Prl, its locus of action, unlike that of dopamine, appears to be somewhere above the MBH-pituitary axis and may involve rostral hypothalamic neurons.