The neurobehavioral effects of ethanol range from mild euphoria, anxiolysis and disinhibition to impaired coordination, ataxia, decreased mentation, slurred speech, nausea and vomiting, and finally to respiratory failure, coma and death, depending on the dose imbibed (Schuckit, 1995). The presumed neuromolecular basis for these behavioral effects includes actions on lipids, at high doses, and more direct molecular targets such as enzymes, neurotransmitter receptors, and ion channels at doses that typically produce intoxication in humans (Harris et al., 2008; Vengeliene et al., 2008). While much progress has been made on identifying molecular targets for ethanol, less insight has been gained into how ethanol’s actions at the molecular level may translate to its behavioral and intoxicating effects. The global behavioral effects of ethanol most likely require the integration of a number of functional neuronal areas distributed over the brain that are in constant interaction with each other. It has been suggested that such large scale integration and communication within the brain could be mediated by groups of neurons that oscillate within a specific frequency range and enter into precise phase-locking, or synchrony,
