Naltrexone-induced LH release in ovariectomized estrogen-primed rats.

In order to investigate the physiological role of endogenous opioid substances in the regulation of gonadotropin secretion, we studied the effect of Naltrexone (Nalt), a morphine antagonist, on serum luteinizing hormone(LH) concentrations in ovariectomized estrogen-treated rats. The site of action of Nalt and its interaction with other putative neurotransmitters on LH secretion were investigated in hypothalamic deafferentated rats and in animals treated with pharmacological inhibitors of the actions of neurotransmitter substances. Nalt injection increased serum LH levels at dosed 0.08 to 2 mg/kg BW. The response was dose-dependent but higher doses of Nalt had less effect. In inducing this response pattern, mediobasal connection between the anterior hypothalamus and the mediobasal hypothalamus was essential, but posterior input to the mediobasal hypothalamus was not necessary. Excepting alpha-adrenergic blocker, all the blockers used, i.e beta-adrenergic, serotonin, dopamine and acetylcholine blockers were effective in eliminating the LH release evoked by Nalt injection. These results suggest that endogenous opioid substances might inhibit LH secretion tonically through aminergic and/or cholinergic neurons and that the mediobasal neural connections to the mediobasal hypothalamus are indispensable for this inhibition.