Other brain regions involved in alcohol-induced memory impairments
        The hippocampus is not the only structure involved in memory formation. A host of other brain structures are also involved in memory formation, storage, and retrieval (Eichenbaum 2002). Recent research with humans has yielded compelling evidence that key areas of the frontal lobes play important roles in short-term memory and the formation and retrieval of long-term explicit memories (e.g., Shastri 2002; Curtis and D'Esposito 2003; Ranganath et al. 2003). Damage to the frontal lobes leads to profound cognitive impairments, one of which is a difficulty forming new memories. Recent evidence suggests that memory processes in the frontal lobes and the hippocampus are coordinated via reciprocal connections (Wall and Messier 2001; Shastri 2002), raising the possibility that dysfunction in one structure could have deleterious effects on the functioning of the other.
       Considerable evidence suggests that chronic alcohol use damages the frontal lobes and leads to impaired performance of tasks that rely on frontal lobe functioning (Kril and Halliday 1999; Moselhy et al. 2001). "Shrinkage" in brain volume, changes in gene expression, and disruptions in how performing certain tasks affects blood flow in the brain have all been observed in the frontal lobes of alcohol-dependent subjects (Kril and Halliday 1999; Lewohl et al. 2000; Tapert et al. 2001; Kubota et al. 2001; Desmond et al. 2003).
      Although much is known about the effects of chronic (i.e., repeated) use of alcohol on frontal lobe function, little is known about the effects of acute (i.e., one-time) use of alcohol on activity in the frontal lobes, or the relationship of such effects to alcohol-induced memory impairments. Compelling evidence indicates that acute alcohol use impairs the performance of a variety of frontal lobe-mediated tasks, like those that require planning, decisionmaking, and impulse control (Weissenborn and Duka 2003; Burian et al. 2003), but the underlying mechanisms are not known. Research also suggests that baseline blood flow to the frontal lobes increases during acute intoxication (Volkow et al. 1988; Tiihonen et al. 1994), that metabolism in the frontal lobes decreases (Wang et al. 2000), and that alcohol reduces the amount of activity that occurs in the frontal lobes when the frontal lobes are exposed to pulses from a strong magnetic field.  Although the exact meaning of these changes remains unclear, the evidence suggests that acute intoxication alters the normal functioning of the frontal lobes (Kahkonen et al. 2003). Future research is needed to shed more light on this important question. In particular, research in animals will be an important supplement to studies in humans, affording a better understanding of the underlying prefrontal circuitry responsible for alcohol-induced memory impairments.