from pre-synaptic terminals via a PKA-dependent mechanism that liberates Ca2+ from internal stores and does not require EC synthesis (Kelm et al., 2007). However, activation of CB1 blocks the enhancement IPSC frequency by ethanol in these neurons leading the authors conclude that this is likely due to the Gi-mediated inhibition of PKA produced by CB1 activation (Kelm et al., 2008). In vivo studies in FAAH KO mice also suggest that AEA opposes some of the acute effects of ethanol including loss of righting reflex and hypothermia while exacerbating others (i.e. hypothermia; Basavarajappa et al., 2006; Vinod et al., 2008a). These results suggest that the EC system interacts with the effects of ethanol in region dependent manner.
