Exercise Enhances Hippocampal Recovery following Binge Ethanol Exposure

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.

Adolescent binge ethanol exposure alters specific forebrain cholinergic cell populations and leads to selective functional deficits in the prefrontal cortex

“…Previous studies have found that non- pharmacological treatments, such as exercise, can reverse both structural and functional deficits related to EtOH exposure (Thomas et al, 2008; Leasure and Nixon, 2010; Maynard and Leasure, 2013; Gallego et al, 2015). Exercise, via the upregulation of neurotrophins, could serve as a protective measure against EtOH’s effects on cognition by re-establishing normal cholinergic/nestin populations, well into adulthood (Gomez-Pinilla and Hillman, 2013; Vivar et al, 2013; Hall et al, 2014).…”

Wheel running reduces ethanol seeking by increasing neuronal activation and reducing oligodendroglial/neuroinflammatory factors in the medial prefrontal cortex

“…With respect to wheel running-induced neuroadaptations in ethanol-experienced subjects, concurrent or delayed access to wheel running inhibits ethanol-induced reduction in hippocampal neurogenesis, and expression of hippocampal trophic factors, suggesting a neuroprotective effect (Crews et al, 2004, Maynard and Leasure, 2013, Gallego et al, 2015). This protection could assist with reduction in certain somatic signs of ethanol withdrawal in animals that experienced wheel running during or after ethanol exposure (Leasure and Nixon, 2010, Devaud et al, 2012, McCulley et al, 2012).…”

Quantitative 3-D analysis of GFAP labeled astrocytes from fluorescence confocal images

“…Our computational method was evaluated on images from three different laboratories. In this paper, we primarily report results from the data acquired in a previously published study of binge alcohol exposure and voluntary exercise (Maynard and Leasure, 2013). Following intracardial perfusion with saline and 4% paraformaldehyde, brains were removed and post-fixed overnight.…”