pancreas. The cerebellar enrichment is particularly relevant with respect to the known effects of alcohol on this brain region: ethanol is the most common injurious agent to Purkinje cells (58, 59). In this context, inter-individual variability in the genetic regulation of cerebellum may be linked to the ability to drink large amounts of alcohol. Additionally, alcohol affects the type-A γ-aminobutyric acid (GABAA) receptor, which mediates autocrine signaling mechanisms in pancreatic cells (60). Individuals with high resistance to the effects of ethanol on this system may be able to drink larger amounts of alcohol; subjects at risk for alcohol dependence tend to have lower levels of response to measures including body sway (61) which is presumably at least in part cerebellar in origin. In a mouse model, it was demonstrated that genetically-influenced differences in cerebellar alcohol response affect alcohol consumption (62). eQTL analysis provide further evidence for functional effects of risk loci, particularly those mapped to chromosome 17, in central nervous system, particularly cerebellum.
