The effect of hyperprolactinemia produced by transplantable pituitary MtTW15 tumor cells in male rats on hypothalamic luteinizing hormone-releasing hormone release in vitro: effects of naloxone and K+.
Although hyperprolactinemia has been reported to decrease reproductive function in male rats, the mechanism of these effects is not fully understood. We examined the effects of chronic hyperprolactinemia and castration on the LHRH content of the medial basal hypothalamus (MBH) and on the basal and evoked in vitro release of LHRH from the MBH-preoptic area (POA). Adult Wistar-Furth male rats were inoculated with MtTW15 tumor fragments; 3 weeks later half of the rats were castrated. Hyperprolactinemic (H) and normoprolactinemic (N) rats were decapitated 2 weeks later to measure MBH LHRH and serum PRL and LH levels. Elevated PRL levels (greater than 2 micrograms/ml) resulted in significantly increased MBH LHRH stores. Castration caused a 57% depletion of MBH LHRH in N rats; in castrated H rats the MBH LHRH content was also reduced by 40%, a significantly lesser extent. Although serum LH levels in intact H rats were only slightly reduced, postcastration LH hypersecretion was significantly attenuated. In a parallel study, the LHRH release rate was assessed by in vitro perfusion of the MBH-POA. The basal LHRH release rates of intact N and H rats were similar. Castrated N rats released LHRH at a reduced rate (50%; P less than 0.01), whereas in castrated H rats the LHRH release rate was reduced by 20%, which corresponded with the partial depletion of the MBH LHRH content in these rats. To examine the possibility of opiate involvement, LHRH release evoked by two consecutive naloxone (NAL) infusions (1 mg/ml for 30 min) was studied. The two NAL infusions resulted in two similar significant increments of LHRH in the MBH-POA of intact N and H rats. However, castration produced different effects on the NAL-induced LHRH release. First, the second NAL pulse was not effective in stimulating LHRH release from the MBH-POA of N and H castrated rats. Further, the first NAL infusion elicited a significant increase in LHRH output from the MBH-POA of N and H castrated rats, but it was significantly lower in comparison with that in their respective intact counterparts. In addition, the NAL-induced LHRH response was higher from the MBH-POA of castrated H than that in castrated N rats. These studies show that neither basal nor evoked LHRH output in vitro is affected by severe and chronic hyperprolactinemia produced by MtTW15 pituitary tumor cells in intact male rats.(ABSTRACT TRUNCATED AT 400 WORDS)
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D000818:Animals; D007987:Gonadotropin-Releasing Hormone / Q000378:metabolism*; D006966:Hyperprolactinemia / Q000209:etiology / Q000503:physiopathology*; D007031:Hypothalamus / Q000187:drug effects / Q000378:metabolism*; D007033:Hypothalamus, Middle / Q000187:drug effects / Q000378:metabolism; D007986:Luteinizing Hormone / Q000097:blood; D008297:Male; D009270:Naloxone / Q000494:pharmacology*; D009368:Neoplasm Transplantation; D009919:Orchiectomy; D010911:Pituitary Neoplasms / Q000150:complications*; D011188:Potassium / Q000494:pharmacology*; D011301:Preoptic Area / Q000187:drug effects / Q000378:metabolism; D051381:Rats; D011920:Rats, Inbred WF
D007987:Gonadotropin-Releasing Hormone; D009270:Naloxone; D007986:Luteinizing Hormone; D011188:Potassium