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  • Alcohol use is associated with a variety of negative consequences, including heightened likelihood of cognitive impairment, proclivity to alcohol use disorders (AUD), and alterations in the drinker's offspring. Children and rodents exposed to alcohol during pregnancy, or those whose fathers consumed alcohol prior to mating, often exhibit neurodevelopmental, physiological, and behavioral deficits. The present study assessed cognitive function and alcohol intake in male and female rats that were offspring of alcohol-exposed fathers. Adult male rats were exposed to alcohol or vehicle (0.0 or 2.0 g/kg, respectively; twice daily for 2 days followed by a rest day, for a total of eight alcohol or vehicle exposure days), or were left untreated and then mated with non-manipulated females. The offspring were assessed for alcohol intake, via intraoral infusion, followed by cognitive assessment via an alternating T-maze task. The results indicated that paternal ethanol exposure, prior to breeding, resulted in offspring that consumed significantly more ethanol than vehicle or untreated controls. Furthermore, the offspring of alcohol-exposed fathers exhibited a significant failure to initiate and complete the T-maze performance tests. Although, when they did engage in the tests they performed at the level of controls (i.e., 80% correct). The present results add to a growing body of literature suggesting that paternal pre-conception alcohol exposure can have deleterious effects on the offspring. Copyright © 2018 Elsevier Inc. All rights reserved.

  • Restraint stress (RS) induces neurotoxicity in the hippocampus, yet most of the studies have employed protracted RS (i.e., = 21 days). Binge ethanol can induce brain toxicity, an effect affected by age. It could be postulated that RS may facilitate ethanol-induced neurotoxicity, perhaps to a greater extent in adolescent vs. older subjects. We analyzed whether adolescent, adult or middle-aged male rats exposed to five episodes of RS followed, 72h later, by binge ethanol (i.e., two administrations of 2.5 g/kg ethanol) exhibited hippocampal neurotoxicity. Adolescents, but not adult or middle-aged rats, exhibited sensitivity to the neurotoxic effects of ethanol at dorsal CA2, ventral CA3 and ventral DG, and a neurotoxic effect of stress at dorsal CA1. Moreover, the combination of ethanol and stress exerted a synergistic effect upon cell degeneration at ventral CA1 and CA2, which was restricted to adolescents. Ethanol also increased cell degeneration, irrespective of age or stress, in dorsal CA3 and in dorsal DG; and ethanol and stress had, across all ages, a synergistic effect upon cell degeneration at the dorsal CA1. The greater neurotoxic response of adolescents to ethanol, stress, or ethanol+stress can put them at risk for the development of alcohol problems. Copyright © 2019 Elsevier B.V. All rights reserved.

Last update from database: 3/13/26, 4:15 PM (UTC)

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