Prenatal ethanol exposure and opiatergic influence on puberty in the female rat.
Fetal alcohol exposure (FAE) is associated with a variety of physiological and behavioral dysfunctions, including deficits to reproductive function. FAE has also been shown to increase brain beta-endorphin levels. This study sought to determine whether the common delay of the onset of puberty in fetal alcohol-exposed animals could be due to increased opiate inhibition of LH release. Prepubertal female rats were injected with an opiate antagonist, naltrexone, over days 26-29. This naltrexone treatment led to an acceleration of vaginal opening and first estrus in FAE animals; had no effect on chow-fed or pair-fed controls. The vaginal opening and first estrus advancement in FAE animals occurred at a lower body weight indicating independence from growth-promoting effects of the drug treatment. It is concluded that delays in puberty in FAE animals are not directly due to pituitary pathology, but are related, at least in part, to increased inhibition of the LHRH neuron and functional impairment of gonadotrophin secretion.
Creighton-Taylor
J A
JA
Department of Anatomy and Neurobiology, University of Missouri School of Medicine, Columbia 65212.
Rudeen
P K
PK
D000818:Animals; D004971:Estrus / Q000187:drug effects; D000431:Ethanol / Q000008:administration & dosage / Q000494:pharmacology*; D005260:Female; D063647:Fetal Alcohol Spectrum Disorders / Q000150:complications; D007986:Luteinizing Hormone / Q000097:blood; D009270:Naloxone / Q000494:pharmacology; D009271:Naltrexone / Q000494:pharmacology; D011247:Pregnancy; D011297:Prenatal Exposure Delayed Effects; D051381:Rats; D011919:Rats, Inbred Strains; D012741:Sexual Maturation / Q000187:drug effects*; D014621:Vagina / Q000187:drug effects / Q000254:growth & development
D009270:Naloxone; D000431:Ethanol; D009271:Naltrexone; D007986:Luteinizing Hormone