Background Chronic intake of ethanol has been linked to serious health consequences such as cardiac and liver problems, cognitive impairments, and brain damage. Alcohol’s detrimental effects depend upon the dose, duration and pattern of exposure with binge drinking as one of the most common, but most damaging, patterns of intake. Little is known about the threshold of the damaging effects of alcohol. Therefore, these experiments sought to determine a threshold for brain damage using various markers of neurodegeneration. Methods Adult male Sprague-Dawley rats were administered nutritionally complete liquid diet containing either ethanol (25% w/v) or isocaloric dextrose every 8 hours for either 1 (mean dose: 13.4 ± 0.3 g/kg/day, mean BEC: 336.2 ± 18.8 mg/dl) or 2 days (mean dose: 10.9 ± 0.3 g/kg/day, mean BEC: 369.8 ± 18.1 mg/dl). Based on a known time course of various neurodegeneration-associated events, rats were perfused transcardially immediately following, 2 days after, or 7 days post ethanol exposure. To label actively dividing cells, some animals were injected with BromodeoxyUridine (BrdU) two hours prior to perfusion. Tissue was then analyzed for the presence of BrdU (cell proliferation), FluoroJade B (degenerative neurons), and vimentin (reactive astrogliosis) immunoreactivity. Results One or two days of ethanol exposure failed to alter cell proliferation at any of the time points analyzed. However, significant 2 to 9-fold increases in neuronal degeneration in limbic cortex and clear evidence of reactive gliosis as indicated by a 2 to 8-fold upregulation in vimentin immunoreactivity in the hippocampus were observed following as little as one day of binge ethanol exposure. Conclusions These results indicate that as little as one day (24 hours) of high BEC, binge-like ethanol exposure is enough to elicit signs of alcohol-induced brain damage in adult rats. Further, reactive gliosis may be a more sensitive marker of alcohol-induced damage in the hippocampus.