Effect of Prenatal Ethanol and Stress on Levels of β‐Endorphin in Different Brain Regions of the Rat

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Abstract
The combination of prenatal ethanol exposure and footshock stress was investigated for its effects on brain β‐endorphin levels. Subjects were offspring of rats that received 1 of 3 prenatal dietary treatments: an ethanol‐containing liquid diet, a identical liquid diet with ethanol substituted isocalorically with maltose‐dextrin (pair‐fed group), and standard laboratory rat chow (chow‐fed group). Two different stress paradigms were used: a short (30‐sec) footshock stress paradigm and a prolonged (180‐sec) footshock stress paradigm. Levels of β‐endorphin were measured with radioimmunoassay in eight brain regions of unstressed (baseline) rats, and of stressed rats at 3 and 30 min following termination of the stress. Seven brain regions containing high densities of β‐endorphin axons and terminals were chosen, as well as the arcuate region of the hypothalamus, the only brain region where bothβ‐endorphin perikarya and terminals are located. Following the short footshock stress paradigm, there were no changes in β‐endorphin levels, except for a trend toward increased levels in the pair‐fed group. After the prolonged stress paradigm, levels of β‐endorphin in both the pair‐fed and chow‐fed groups tended to be decreased in several brain regions, including the arcuate region, at 3 min after termination of the stress. In contrast, for the prenatally ethanol‐exposed group, β‐endorphin levels were increased significantly in the arcuate region, and moderately increased in the septal/preoptic region and medulla/pons at 3 min after the prolonged stress paradigm. In the hypothalamus, there was a modest decrease in β‐endorphin levels in all three treatment groups, and little change in β‐endorphin levels at any time after stress in the amygdala, thalamus, and midbrain regions. The decrease in peptide levels in pair‐fed and chow‐fed rats following stress is interpreted as release of the peptide from terminal stores. The failure of the prenatally ethanol‐exposed group to demonstrate this release in the arcuate region, the septal/preoptic region, and the medulla/pons may be related to loss of homeostatic control, seen in behavioral studies of prenatally ethanol‐exposed rats, and in human children with the fetal alcohol syndrome.