Overview and introduction

Overview
       Alcohol interferes with the ability to form new memories.  Large amounts of alcohol, particularly if consumed rapidly, can produce partial (i.e., fragmentary) or complete (i.e., en bloc) blackouts, which are periods of memory loss for events that transpired while a person was drinking.  Blackouts have long been associated with alcoholism.  However, recent studies (e.g., White et al., 2002; White et al., in press 2004; White, in press 2004) indicate that blackouts are much more common among social drinkers, including college drinkers, than was previously assumed.  While often confused with passing out, or losing consciousness after excessive drinking, blackouts do not involve a loss of consciousness.  Indeed, individuals can engage in a wide range of goal-directed, voluntary, often complicated behaviors during blackouts -- from driving cars to having sexual intercourse (White et al., 2002).  Alcohol has only a minimal impact on the ability to remember information learned before becoming intoxicated or on keeping information active in memory for short periods of time.  For these reasons, outside observers are often unaware of the individual's true level of intoxication.  The history and current status of research regarding alcohol-induced blackouts, including knowledge of the brain mechanisms involved, will be reviewed below.

Introduction
      If recreational drugs were tools, alcohol would be a sledgehammer. Few cognitive functions or behaviors escape the impact of alcohol, a fact that has long been recognized in the literature.  As Fleming (1935) stated nearly 70 years ago, "The striking and inescapable impression one gets from a review of acute alcoholic intoxication is of the almost infinite diversity of symptoms that may ensue from the action of this single toxic agent."  In addition to impairing balance, motor coordination, decision making, and a litany of other functions, alcohol is a potent amnestic agent.  Beginning with just one or two drinks, alcohol produces detectable memory impairments.  As the dose increases, so does the magnitude of the memory impairments.  The purpose of this review is to discuss what is currently known regarding the behavioral correlates and pharmacological mechanisms underlying acute alcohol-induced memory dysfunction.