Effects of opiate antagonists on serotonin turnover and on luteinizing hormone and prolactin secretion in estrogen- or morphine-treated rats.

Previous findings indicate that estradiol benzoate (EB) acutely activates serotonergic projections in the medial preoptic area that are stimulatory to prolactin (PRL) secretion. Because opioid agonists also stimulate both PRL release and serotonin (5-HT) turnover, the present experiments tested whether endogenous opioid neurons may mediate estrogen feedback effects. In experiment 1, ovariectomized rats received either 50 micrograms EB or oil vehicle, and either saline or a long-acting opiate receptor blocker, nalmetrene (10 mg/kg), simultaneously, 3 h prior to decapitation. The pargyline method was used to determine 5-HT turnover; hence members of each treatment group received either saline or pargyline (75 mg/kg i.p.) 30 min prior to decapitation. Plasma PRL and luteinizing hormone (LH) concentrations were determined by radioimmunoassays, and 5-HT concentrations from microdissected, individual brain nuclei were measured by liquid chromatography with electrochemical detection. Nalmetrene blocked both the acute elevation of PRL and the increase in 5-HT turnover in the medial preoptic nucleus and ventromedial nucleus induced by EB. Nalmetrene alone also enhanced LH release and 5-HT turnover in the bed nucleus of the stria terminalis, and these effects were prevented by EB. A second study tested whether the opioid agonist, morphine, mimics estrogen effects on PRL and preoptic 5-HT turnover. Animals received saline, morphine (10 mg/kg i.p.) and/or naloxone (5 mg/kg i.p.) 30 min prior to decapitation. Simultaneously, half in each group received pargyline as above.(ABSTRACT TRUNCATED AT 250 WORDS)