Dopaminergic and Opioid Compounds

Le résumé fourni par la source

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.

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