Prenatal Exposure to Ethanol Alters the Ontogeny of the β‐Endorphin Response to Stress

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Abstract
To determine whether prenatal exposure to ethanol alters the response of the β-endorphin (β-EP) system to stress, the effect of two types of stressful stimuli, ether and cold, was examined in the offspring of rats which during pregnancy were: (a) fed with an ethanol-containing diet; (b) pair-fed with an isocaloric sucrose diet; and (c) fed ad libitum with standard lab chow (basic control group). The effect of stress on the content of β-EP in the serum, pituitary gland and hypothalamus, as well as on the serum corticosterone and hypothalamic corticotropin-releasing factor (CRF) content was examined. Pups prenatally exposed to ethanol had significantly higher serum β-EP levels on Day 1 and higher serum corticosterone levels on Days 1-3 when compared to their pair-fed or basic controls. On all days tested pituitary β-EP content was lower in the offspring of the ethanol-treated rats than in the control groups. There was no difference in the total hypothalamic β-EP content between the three treatment groups; however, during the first 10 days of life a higher concentration (ng/mg protein) of β-EP was observed in the hypo-thalami of the ethanol and the pair-fed group when compared to the basic control pups. Hypothalamic CRF levels, though significantly lower in the pups exposed to ethanol in utero than in the control groups on Day 3, increased significantly in the ethanol group between Days 14 and 22, while no significant change was observed during this period in either of the control groups. From Days 1 to 10 significant elevations in serum corticosterone, levels were observed following both types of stress in the pair-fed and the basic control group, while no significant response, to either type of stressful stimuli, was observed prior to Day 14 in the pups exposed to ethanol prenatally. On Day 14 cold stress induced small increases in the serum β-EP and corticosterone levels of the offspring treated prenatally with ethanol which, however, were less pronounced than the elevations observed in both of the control groups. Furthermore, exposure to ether stress on Day 14 elicited no response by the β-EP system of the ethanol-exposed offspring. In contrast, the 22-day-old offspring of the ethanol-treated rats exhibited greater elevations in serum β-EP and corticosterone levels, following stress, than the offspring of the pair-fed and basic control groups. The elevations of serum β-EP levels following stress were associated with small decreases in the pituitary β-EP and hypothalamic CRF contents. Thus, the response of the β-EP system to stress was modified by prenatal exposure to ethanol, being suppressed at early postnatal life and enhanced at later stages of development. The transition from reduced to enhanced responsiveness seemed to occur during the third week of life.