Abstract
Binge drinking damages the brain, and although a significant amount of recovery occurs with abstinence, there is a need for effective strategies to maximize neurorestoration. In contrast to binge drinking, exercise promotes brain health, so the present study assessed whether it could counteract ethanol-induced damage by augmenting natural self-repair processes following one or more binge exposures. Adult female rats were exposed to 0 (control), 1 or 2 binges, using an established 4-day model of binge-induced neurodegeneration. Half of the animals in each group remained sedentary, or had running wheel access beginning 7 days after the final binge, and were sacrificed 28 days later. To assess binge-induced hippocampal damage and exercise restoration, we quantified volume of the dentate gyrus and number of granule neurons. We found that a single binge exposure significantly decreased the volume of the dentate gyrus and number of granule neurons. A second binge did not exacerbate the damage. Exercise completely restored baseline volume and granule neuron numbers. To investigate a potential mechanism of this restoration, we administered IdU (a thymidine analog) in order to label cells generated after the first binge. Previous studies have shown that neurogenesis in the dentate gyrus is decreased by binge alcohol exposure, and that the hippocampus responds to this insult by increasing cell genesis during abstinence. We found increased IdU labeling in binge-exposed animals, and a further increase in binged animals that exercised. Our results indicate that exercise reverses long-lasting hippocampal damage by augmenting natural self-repair processes.
Highlights
Binge drinking is a common alcohol use disorder (AUD) in the United States – one in six American adults reports binge drinking four times a month [1]
Animal models of binge alcohol consumption replicate the pattern of brain damage seen in binge drinking humans [13,14,15,16], and provide a means by which to systematically study the mechanisms of alcohol-induced neuronal damage and endogenous self-repair processes, as well as test potential therapeutic interventions
Such studies show that binge alcohol exposure kills cells [13] and decreases neurogenesis in the dentate gyrus (DG), a neurogenic region of the adult central nervous system [17,18]
Summary
Binge drinking is a common alcohol use disorder (AUD) in the United States – one in six American adults reports binge drinking four times a month (eight drinks per binge) [1]. Animal models of binge alcohol consumption replicate the pattern of brain damage seen in binge drinking humans [13,14,15,16], and provide a means by which to systematically study the mechanisms of alcohol-induced neuronal damage and endogenous self-repair processes, as well as test potential therapeutic interventions. Such studies show that binge alcohol exposure kills cells [13] and decreases neurogenesis in the dentate gyrus (DG), a neurogenic region of the adult central nervous system [17,18].
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