Historically, astrocyte activation has been defined by glial fibrillary acidic protein (GFAP) upregulation, although this is an oversimplification (Oberheim et al. 2012). GFAP levels increase in response to acute stressors like ischaemia and neurotoxins. Acute and chronic ethanol exposure in rats dose-dependently increases GFAP expression in several brain regions (Vongvatcharanon et al. 2010; Udomuksorn et al. 2011). However, with chronic ethanol exposure, GFAP downregulation and astrocyte cell death have been observed (Khokhrina et al. 1991). Miguel-Hildago and colleagues confirmed decreased astrocyte density in the dorsolateral and orbitofrontal cortices of alcoholics without Wernicke-Korsakoff syndrome (Miguel-Hidalgo et al. 2002, 2006). In contrast, astrocyte density increases with age and in long-standing alcoholism, which may represent gliosis due to chronic neurotoxicity (Miguel-Hidalgo et al. 2006).
