In contrast to the findings mentioned above, there is also evidence that acute ethanol inhibits EC signaling in a number of brain regions. Direct measures of EC tissue content have found that acute or short-term exposure to ethanol reduces EC levels in the hippocampus, striatum, prefrontal cortex, amygdala, and cerebellum (Ferrer et al., 2007; Rubio et al., 2007). Futhermore, these reductions in EC levels are not associated with enhanced FAAH activity (Ferrer et al., 2007; Rubio et al., 2009) suggesting that the effects of acute and short-term ethanol are not mediated by increased metabolism.
