Research Reports - Binge ethanol in adulthood exacerbates negative outcomes following juvenile traumatic brain injury

Brain Behav Immun. 2017 Feb;60:304-311. doi: 10.1016/j.bbi.2016.11.009. Epub 2016
Nov 12.

Karelina K(1), Gaier KR(2), Prabhu M(2), Wenger V(2), Corrigan TE(2), Weil ZM(2).

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. 

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