Naloxone administration to female hamsters advances puberty by enhancing luteinizing hormone release.
In the female hamster, a daily rhythm of gonadotropin release begins almost 3 weeks prior to the initiation of 4-day estrous cycles. A temporal relationship exists between the onset of this cyclic release of gonadotropin and age at puberty. We hypothesized that since opiate agonists depress circulating gonadotropins and antagonists increase them in both adult and immature rodents, endogenous opiates may influence the mechanism controlling cyclical gonadotropin release in the prepubertal female hamster and thus affect rate of sexual maturation and hence the age at puberty. This proposal was tested by chronic administration of naloxone (NAL), an opiate receptor antagonist. We predicted that NAL might induce the early initiation of daily surges of luteinizing hormone (LH) if endogenous opiates inhibit sexual maturation. Naloxone was injected daily (50 mg/kg body wt) at about 1300 hr from Days 1 through 17 of age. The NAL injections increased serum LH and significantly advanced the age at which first estrus vaginal discharge was observed (32 vs 38 days for saline-injected controls in Experiment I and 31 vs 37 days in Experiment II). However, the NAL injections did not correspondingly advance the age of initiation of endogenously generated daily cycles of circulating LH. We conclude that blockade of opiate receptors accelerates sexual maturation by directly inducing the release of LH and not by advancing the age of initiation of endogenous gonadotropin surges.
D000367:Age Factors; D000818:Animals; D006224:Cricetinae; D005260:Female; D007986:Luteinizing Hormone / Q000378:metabolism*; D008647:Mesocricetus; D009270:Naloxone / Q000494:pharmacology*; D010060:Ovulation / Q000187:drug effects
D009270:Naloxone; D007986:Luteinizing Hormone