Studies conducted so far suggest that there are several common substrates (e.g., theta oscillations, beta oscillations, P3 amplitude) that are influenced by alcohol in both acute and chronic use and this in turn may reflect the underlying vulnerability of the brain to alcohol. The potential to isolate genetic underpinnings of impaired neuroelectrophysiological features associated with alcohol use is another exciting direction that may provide viable targets for intervention. Although no functional variant affecting the neuroelectrophysiological characteristics has yet been identified at the molecular level, a large body of pharmacological evidence attests to the relevance of these receptors for aspects of cognitive function. This approach has the unprecedented potential to unravel the complex interplay of various neural subsystems relevant to the generation of brain oscillations elicited under different cognitive conditions and in disease states.
