One of the most consistent findings in alcohol-exposed rodents, ventricular enlargement, varies with timing and method of alcohol exposure. It is far more pronounced in rats achieving average blood alcohol levels (BALs) of 250 mg/dL in just 4 days of involuntary binge-type administration of EtOH (Zahr et al. 2010, 2013, 2014b) than in rats achieving average BALs of 200 mg/dL over 24 weeks using vapor EtOH exposure (Pfefferbaum et al. 2008) or P rats gradually achieving average BALs of 125 mg/dL with voluntary EtOH consumption (Pfefferbaum et al. 2006a), where only modest ventricular enlargement was noted (cf., Fadda and Rossetti 1998; Nixon 2006). Even repeated binge exposures (i.e., 5 cycles of 4 days of intragastric binge EtOH exposure with 1 week abstinence in between), do not result in persistent effects on the brain detectable with MRI (Zahr et al. 2015). Although ventricular size increases with each binge EtOH exposure, there is rapid recovery during each week of abstinence (Zahr et al. 2015). Such studies suggest that EtOH alone, at least in the exposure protocols evaluated with MRI, does not result
