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 specific reductions in expression (Ortiz et al., 2004). Another dependence study in rats, found that hippocampal expression of CB1 mRNA and protein was reduced following chronic intermittent treatment with ethanol, and these changes in expression corresponded with reduced physiological measures of CB1-mediated inhibition of GABAergic synaptic transmission indicating a loss of function as well (Mitrirattanakul et al., 2007). Importantly, this study also reported that CB1 expression rebounded above control levels following 40 days of withdrawal, and similar results have been reported for CB1 expression in the cingulate cortex following a 3 week withdrawal from chronic ethanol treatment (Rimondini et al., 2002). Despite these reports, Gonzalez et al (2002) found no change in CB1 binding or gene expression in any of fifteen brain regions examined, including cingulate cortex, hippocampus, dorsal striatum, NAc, BLA, and cerebellum. In this study, rats were treated with ethanol (7.2%) via a liquid diet for 15 days prior to tissue collection, but the BECs obtained by these
