Preclinical studies have demonstrated that pre-frontal cortex (PFC) GFAP-immunoreactive cell density is lower in alcohol-naive and alcohol-preferring rats relative to non-alcohol-preferring rats (Miguel-Hidalgo 2005) (see Table I). Glial cell dysfunction also predates alcohol exposure in this susceptible rodent strain. In the adult rat medial PFC, binge-like alcohol administration during adolescence decreases glial density without affecting neuronal density in male but not female rodents and without affecting cell density in the basolateral amygdala (Koss et al. 2012). However, earlier bingelike alcohol exposure increases bromodeoxyuridine-labelled (dividing) cells; 60% of these cells express glial markers into adulthood (Helfer et al. 2009). Moreover, gliotoxin or gap junction blocker infusion into the prelimbic cortex transiently increases alcohol self-administration (Miguel-Hidalgo et al. 2009; Miguel-Hidalgo 2007). In contrast to these preclinical findings, a postmortem study of alcohol-dependent depressed suicide completers revealed increased glial packing density in the anterior cingulate cortex (ACC) relative to non-alcoholic individuals with depression who committed suicide as well as sudden (non-suicide) deaths (Hercher et al. 2009). Taken together, the results suggest that altered astrocyte density may be a cause instead of a consequence of alcoholism.
