Given the CNS depressant effects of ethanol, the ability of acute ethanol administration to activate release of ECs seems, at first, to be contradictory as synthesis and release of ECs are highly dependent on excitability-induced elevations intracellular Ca2+ concentrations. However, brief incubation with ethanol is known to increase intracellular Ca2+ in forebrain synaptosomes (Davidson et al., 1988) and in hippocampal neurons via release from intracellur stores (Mironov and Hermann, 1996). Along these lines, several pieces of evidence suggest that the effects of acute ethanol are mediated in part by the liberation of ECs from neural tissue and their subsequent actions on neurotransmission (table 1). Basavarajappa et al (2008) found that a 30 min application of 50 mM ethanol (approximately 200 mg %) was sufficient to increase both AEA and 2-AG in hippocampal cultures and that this increase in EC content was Ca2+-dependent. Furthermore, these authors reported that the ethanol-mediated increase in EC levels resulted in reduced pre-synaptic glutamate release. Additional evidence comes from in vivo studies where SR or chronic pre-treatment with the CB1 agonist, WIN 55,212-2 (WIN), reduced the
