The effects of acute i.v. administration of gonadotrophin-releasing hormone (GnRH; 0·1 μg/kg), morphine (3 mg/kg) and/or naloxone (0·5 mg/kg) on LH and FSH secretion was evaluated in young male pigs (approximately 6 weeks old) with venous brachiocephalic cannulae. The effects of morphine and/or naloxone treatments on prolactin and GH were also evaluated. The influence of morphine on hypophysial hormone secretion was also examined 2 days after castration. Animals treated with morphine and/or naloxone were compared with saline-injected control animals. Injection of GnRH induced 400 and 50% increases in LH and FSH respectively. Morphine and/or naloxone did not influence LH secretion in intact or castrated animals. Morphine suppressed (P < 0·01) FSH levels 40–60 min after injection whereas naloxone had no effect. Castration eliminated morphine-induced suppression of FSH. Injection of morphine followed by naloxone resulted in acutely raised (P < 0·05) FSH concentrations. Morphine induced a threefold increase (P < 0·01) in prolactin within 30 min of injection and naloxone inhibited the effect of morphine. Levels of GH were increased (P < 0·01) 20 min after morphine treatment and this increase was delayed when naloxone was given immediately after morphine. Naloxone alone did not affect prolactin or GH secretion. Castration caused increases in LH (P < 0·05) and FSH (P < 0·01), did not influence prolactin or GH, and reduced plasma testosterone to undetectable (< 1·0 nmol/l) levels. These results suggest that in young male pigs the hypothalamic-hypophysial axis is responsive to GnRH and gonadal negative feedback. The opiate/LH pathway appears to be non-functional or incomplete, while the opiate/FSH pathway seems to be active. Morphine stimulated the release of prolactin probably via a naloxone-sensitive opiate receptor.
J. Endocr. (1988) 119, 501–508
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