The neurophysiological consequences of intoxication with ethanol and cannabinoids are now understood to arise from the interaction of these substances with specific molecular substrates, particularly with membrane bound receptors and enzymes. Cannabinoid drugs interact specifically with the components of the EC system to modulate neurotransmission primarily at glutamatergic and GABAergic synapses. In contrast, the molecular substrates with which ethanol interacts are numerous and vary greatly with regard the neurochemical processes they participate in. However, mounting evidence from biochemical, genetic, electrophysiological, and behavioral studies conducted over the past decade indicates that the EC system plays an important role in mediating the acute effects of ethanol. Furthermore, the function of the EC system is perturbed following chronic exposure to ethanol, and these data suggest that altered EC signaling may contribute to the underlying neuropathology that drives alcohol abuse and dependence disorders. The remainder of this review will focus specifically on the interactions between ethanol and the EC system.
