Opioid Effects on Plasma Concentrations of LuteinizingHormone and Prolactin in the Adult Male Rhesus Monkey*

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Abstract
The role of endogenous opioid peptides (EOP)in the neuroendocrine control of primate gonadotropin and PRLsecretion was studied in nonrestrained adult male rhesus monkeys.Morphine (0.5β1.0 mg/kg) was used as the prototypeopiate, β-endorphin (β-END; 10-20 μg/kg) and [D-Ala2,D-Leu5]enkephalin (DADLE; 5β20 mg/kg) were used as representativesof EOP, and naloxone (0.5β2.0 mg/kg) was used as an opiatereceptor blocker. Drugs were administered and blood was collected(at 20-min intervals for 4 h) through an indwelling jugularcatheter. LH and PRL levels were measured in plasma by RIA. Intravenous administration of morphine (1.0 μg/kg) and DADLE (10 g/kg) produced decreases in LH levels of 64% and40%, respectively. These decreases occurred within 1 h afterdrug injections and lasted for approximately 3 h. (β-END had noeffect on LH levels. Naloxone, at all doses studied, significantlyincreased LH levels (5- to 8-fold). The LH rises occurred within20 min and lasted for up to 2 h. Both morphine and β-END produced immediate increases in PRL, which remained elevatedfor 3 h. DADLE did not alter PRL levels. Naloxone (1.0 and 2.0mg/kg) decreased PRL concentrations (45% and 60%, respectively). Pretreatment with morphine or DADLE did not alter the LHresponse to GnRH (100 μg) stimulation, indicating a hypothalamicsite of action for the opioid inhibition of LH release.Naloxone administration reversed the inhibitory effects of morphineand DADLE on LH. The stimulatory effect of morphineon PRL levels was also reversed by naloxone. These studiesfurther define the postulated physiological role of EOP in primatereproductive neuroendocrinology. Based on receptor selectivities of these opioid agonists, the inhibition of LH may bemediated by Δ-receptors, whereas PRL release appears to be μmediated.