Browsing by Author "Maynard, Mark E."
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Item Can Exercise Reverse Binge Alcohol-Induced Brain Damage?(2013-05) Maynard, Mark E.; Leasure, J. Leigh; Hernandez, Arturo E.; Yoshida, HanakoBinge pattern drinking is characterized by excessive alcohol intake, combined with multiple periods of intoxication and withdrawal. This excessive consumption produces gray and white matter cell loss and cognitive impairments, leading to a cycle of further alcohol consumption. Animal models implicate the hippocampus, important for learning and memory, as being particularly sensitive to alcohol induced-neurodegeneration. Furthermore, binge alcohol has been shown to induce cell death and inhibit adult neurogenesis. Voluntary running-wheel exercise has been shown to increase hippocampal neurogenesis and promote overall brain health. The current study investigates the effects of repeated binge alcohol exposure and the potential of voluntary exercise to aid in recovery during abstinence. Female Long Evans rats were exposed to 1 or 2 four-day binge alcohol exposures before exercising voluntarily for four weeks. Rats were sacrificed 35 days after their last dose of alcohol and examined for histological markers of neurogenesis (doublecortin (DCX+)) and cell survival, (number of remaining granule cells) in the dentate gyrus. Binge exposure resulted in a decrease in granule cells, an effect that was reversed by exercise. A single binge had no effect on DCX+ cells; however, a second binge significantly reduced the number of DCX+ cells. Exercise increased the number of DCX+ cells in controls, however there was no increase in single binge animals demonstrating a binge induced suppression of the neurogenic effect of exercise. We conclude that while exercise can restore binge alcohol induced loss of granule cells, repeated binge alcohol exposure decreases neuronal differentiation in the hippocampus after 5 weeks of abstinence. Exercise, which promotes neurogenesis in the alcohol-naïve brain, may have limited ability to do so in the binge-exposed brain.Item Exercise enhances hippocampal recovery following binge ethanol exposure(PLoS ONE, 2013-09) Maynard, Mark E.; Leasure, J. LeighBinge 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.Item Sex Differences in Binge Alcohol-Induced Brain Damage and Recovery of Function(2016-05) Maynard, Mark E.; Leasure, J. Leigh; Neighbors, Clayton; Roman, Gregg; Roysam, BadrinathEvidence suggests that women are more sensitive to the neurotoxic effects of alcohol and more vulnerable to the adverse medical consequences of heavy alcohol consumption than men. Despite this few studies have directly compared the consequences of binge alcohol between the male and female brain, and the mechanisms that underlie increased female vulnerability remain poorly understood. The present studies investigated sex differences in alcohol-induced neurodegeneration, and associated cognitive deficits and disruption of trophic support, using a rodent model of an alcohol use disorder (AUD). Binge exposure resulted in a significant loss of granule neurons and significantly more degenerating and dead cells in the hippocampal dentate gyrus of females compared to males. This was associated with a binge-induced spatial reference memory deficits in the Morris water maze for females but not males. Binge-induced neurodegeneration in the female hippocampus was associated with a decrease of BDNF, TrkB, CREB, and pCREB protein expression; however only BDNF was disrupted in the hippocampus of males. Further, we investigated if exercise-driven recovery from binge-induced neurodegeneration was associated with increased trophic support. One to two weeks of voluntary exercise reversed the binge-induced reduction of dentate gyrus granule neurons in females, likely via an increase in BDNF, pCREB, and Iba1 (microglia). We conclude that the female hippocampus is more sensitive to binge-induced neurodegeneration and associated cognitive consequences than males, like due to the disruption of protective tropic support. Voluntary exercise however, can enhance endogenous recovery processes by increasing trophic support that aids in recovery.