Hungund’s lab was the first to publish that chronic ethanol treatment reduced CB1 expression and function (Basavarajappa et al., 1998; Basavarajappa and Hungund, 1999b). In these studies, mice were exposed chronically to ethanol vapor for three days and then tissue from whole-brain homogenates was assayed for CB1 binding and G-protein coupling. Since these seminal experiments, altered CB1 expression and function have been reported by a number of labs implementing various chronic and sub-chronic ethanol regimens (table 3). Replicating their previous findings, Hungund’s lab reported that 3-day ethanol vapor inhalation produces a down-regulation of CB1 expression and function in mouse cortex, hippocampus, striatum, and cerebellum (Vinod et al., 2006). In another study, sub-chronic administration of ethanol (2 g/kg; twice daily) for 7 days decreased sensitivity to WIN-induced changes in monoamine synthesis in the striatum, hippocampus, and locus coeruleus (Moranta et al., 2006). In addition, rats made ethanol dependent using 52 days of forced access to a 10% ethanol solution had reduced CB1 gene expression in the striatum, hippocampus, and hypothalamus, but expression was not altered in the cingulate cortex suggesting region
