Fetal Exposure to Ethanol Enhances Pituitary‐Adrenal and Temperature Responses to Etanol in Adult Rats

Abstract

Long lasting effects of perinatal ethanol exposure were studied in adult rats who were the offspring of dams fed a 5.0% w/v ethanol-containing liquid diet ad libitum or pair-fed the isocaloric control diet during gestation weeks 2 and 3 or during postnatal week 1. Fetal exposure to ethanol reduced body weight of pups at birth unless the ethanol diet was supplemented with casein; neonatal exposure to the ethanol or pair-fed diets, casein supplemented or not, reduced pup weights until day 21 postnatally when weights of all fetally or neonatally exposed pups were normal. Between 52 and 120 days of age females were tested for pituitary-adrenal and temperature responses to a challenge dose of ethanol. Prenatally ethanol-exposed rats showed significantly higher plasma corticosterone titers and developed a greater hypothermia in response to an intraperitoneal injection of ethanol (0.75--1.5 g/kg) than did pair-fed controls. Similar responses enhancement did not occur in the postnatally ethanol-exposed rats. Temporal patterns of blood ethanol levels after an intraperitoneal injection of ethanol (1.5 g/kg) were similar in prenatally ethanol-exposed females and their pair-fed controls. The data indicate that exposure to ethanol in utero exerts persistent effects on the offspring, rendering them more responsive to the hypothermic and pituitary-adrenal activating effects of alcohol as adults.

Moderate Level Fetal Alcohol Exposure and Serotonin Transporter Gene Promoter Polymorphism Affect Neonatal Temperament and Limbic-Hypothalamic-Pituitary-Adrenal Axis Regulation in Monkeys

“…Also, "anger-prone" 15 month-old infants exhibit augmented CORT response when confronted with a stranger or a frightening robot-toy (48). In rodents, FAexposure leads to either LHPA axis hyper-responsiveness to stressors or delayed or deficient return to pre-stress level (49,50,51,52,53,54,55,56). In this study, the effects of FA-exposure on increased infant irritability and LHPA axis responsiveness were most prominent in rhesus monkeys carrying the s allele.…”

Increased ethanol intake after prenatal ethanol exposure: Studies with animals

“…This relationship seems to be mediated by different hormonal and neurochemical systems, such as the HPA axis and the pituitary Beta-endorphin system. Prenatal ethanol exposure alters levels of adrenocorticotropin hormone (ACTH) and corticosterone (Taylor et al, 1981;Taylor et al, 1988;Weinberg, 1989;Weinberg et al, 1996) as well as Beta-endorphins (Angelogianni and Gianoulakis, 1989) in response to different stressors. As mentioned earlier, in one study higher ethanol consumption was observed in rats prenatally exposed to the drug, but only after chronic stress (Nelson et al, 1983).…”

Acute sensitivity and acute tolerance to ethanol in preweanling rats with or without prenatal experience with the drug

“…When rats are exposed to high ethanol doses throughout the last two weeks of the gestation, long-lasting effects upon the activity of the hypothalamic-pituitary-adrenal axis (HPA) are consistently observed (Taylor, Branch, Liu, & Kokka, 1982;Taylor et al, 1981;Weinberg, Taylor, & Gianoulakis, 1996). This prenatal treatment induces heightened responsiveness to various stressors, a phenomenon that could eventually predispose the organism to use or abuse ethanol as a means of alleviating stressrelated negative states (e.g.…”