Abstract

The combination of prenatal ethanol exposure and footshock stress was investigated for its effects on brain beta-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 beta-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 beta-endorphin axons and terminals were chosen, as well as the arcuate region of the hypothalamus, the only brain region where both beta-endorphin perikarya and terminals are located. Following the short footshock stress paradigm, there were no changes in beta-endorphin levels, except for a trend toward increased levels in the pair-fed group. After the prolonged stress paradigm, levels of beta-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, beta-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.(ABSTRACT TRUNCATED AT 250 WORDS)

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