title: Binge ethanol in adulthood exacerbates negative outcomes following juvenile traumatic brain injury.
abstract: Traumatic brain injuries (TBI) are a major public health problem with enormous costs in terms of health care dollars, lost productivity, and reduced quality of life. Alcohol is bidirectionally linked to TBI as many TBI patients are intoxicated at the time of their injury and we recently reported that, in accordance with human epidemiological data, animals injured during juvenile development self-administered significantly more alcohol as adults than did sham injured mice. There are also clinical data that drinking after TBI significantly reduces the efficacy of rehabilitation and leads to poorer long-term outcomes. In order to determine whether juvenile traumatic brain injury also increased the vulnerability of the brain to the toxic effects of high dose alcohol, mice were injured at 21days of age and then seven weeks later treated daily with binge-like levels of alcohol 5g/kg (by oral gavage) for ten days. Binge-like alcohol produced a greater degree of neuronal damage and neuroinflammation in mice that sustained a TBI. Further, mice that sustained a juvenile TBI exhibited mild learning and memory impairments in adulthood following binge alcohol and express a significant increase in hippocampal ectopic localization of newborn neurons. Taken together, these data provide strong evidence that a mild brain injury occurring early in life renders the brain highly vulnerable to the consequences of binge-like alcohol consumption.
authors.affiliation: Department of Neuroscience, Group in Behavioral Neuroendocrinology and Center for Brain and Spinal Cord Repair, Ohio State University Wexner Medical Center, Columbus, OH 43210, USA. Electronic address: Ekaterina.karelina@osumc.edu.
authors.forename: Kate
authors.initials: K
authors.lastname: Karelina
authors.affiliation: Department of Neuroscience, Group in Behavioral Neuroendocrinology and Center for Brain and Spinal Cord Repair, Ohio State University Wexner Medical Center, Columbus, OH 43210, USA.
authors.forename: Kristopher R
authors.initials: KR
authors.lastname: Gaier
authors.affiliation: Department of Neuroscience, Group in Behavioral Neuroendocrinology and Center for Brain and Spinal Cord Repair, Ohio State University Wexner Medical Center, Columbus, OH 43210, USA.
authors.forename: Maya
authors.initials: M
authors.lastname: Prabhu
authors.affiliation: Department of Neuroscience, Group in Behavioral Neuroendocrinology and Center for Brain and Spinal Cord Repair, Ohio State University Wexner Medical Center, Columbus, OH 43210, USA.
authors.forename: Vanessa
authors.initials: V
authors.lastname: Wenger
authors.affiliation: Department of Neuroscience, Group in Behavioral Neuroendocrinology and Center for Brain and Spinal Cord Repair, Ohio State University Wexner Medical Center, Columbus, OH 43210, USA.
authors.forename: Timothy E D
authors.initials: TED
authors.lastname: Corrigan
authors.affiliation: Department of Neuroscience, Group in Behavioral Neuroendocrinology and Center for Brain and Spinal Cord Repair, Ohio State University Wexner Medical Center, Columbus, OH 43210, USA.
authors.forename: Zachary M
authors.initials: ZM
authors.lastname: Weil
mesh_terms: D000428:Alcohol Drinking / Q000009:adverse effects*; D000818:Animals; D001921:Brain / Q000503:physiopathology*; D001930:Brain Injuries / Q000503:physiopathology*; D000070642:Brain Injuries, Traumatic / Q000503:physiopathology*; D004195:Disease Models, Animal; D000431:Ethanol / Q000009:adverse effects*; D005260:Female; D051379:Mice
chemical_list: D000431:Ethanol
keywords: Alcohol; Axon degeneration; Learning and memory; Microglia; Neurogenesis; Neuroinflammation; Traumatic brain injury