Mounting evidence suggests that ethanol arrests the expression of behavioral variability. A measure of diversity and unpredictability in normal behavior seems critical for the adjustment to changes in the causal texture of the environment, and its deletion by ethanol may, in man, contribute to the compulsive drinking and stereotyped behavior associated with alcohol abuse and alcoholism. These considerations lend significance to our long term goals of securing ethanol's status as a general, nonspecific agent of invariance whose effect on variability is direct and not secondary to impairment of other behavioral or cognitive processes. If these aims can be realized, and if we come to an understanding of the CNS structures and transmitters involved, this compulsive effect of ethanol might be susceptible to selective pharmacological blockade, or CNS resistance to it might be conferred by environmental or developmental intervention. Barring this, it is not inconceivable to suppose that those at high risk for ethanol stereotypy could be identified in advance by innocuous neurological or pharmacological probes. The goals of the proposed animal studies are threefold and include the display of behavioral variability along the new dimensions of context approach, response duration, response rhythmicity, and spatial dispersion. The extent of suppression of each by ethanol will be carried out in a dose-response design employing a specially modified operant system and a parallel arm maze. Second, two competing interpretations of the variability work are critically evaluated. An impairment in spatial guidance or in working memory could produce a secondary stereotypy. Thus, the issue of direct vs. indirect ethanol effects are addressed in rigorous designs employing radial-arm mazes, a water maze, and parallel maze that are capable of assessing each possibility independently. Finally, our present work encourages us to think that we can more accurately pinpoint the CNS site and neurotransmitter through which ethanol exerts its effect on variability. Selective damage or cholinergic dennervation of forebrain structures is inflicted in an effort to locate circuits that mediate or oppose the expression of the ethanol effects under study.