What happened? Alcohol, memory blackouts, and the brain

Abstract

Alcohol primarily interferes with the ability to form new long-term memories, leaving intact previously established long-term memories and the ability to keep new information active in memory for brief periods. As the amount of alcohol consumed increases, so does the magnitude of the memory impairments. 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 are much more common among social drinkers--including college drinkers--than was previously assumed, and have been found to encompass events ranging from conversations to intercourse. Mechanisms underlying alcohol-induced memory impairments include disruption of activity in the hippocampus, a brain region that plays a central role in the formation of new autobiographical memories.

Figures

Figure 1

A general model of memory formation, storage, and retrieval based on the modal model of memory originally proposed by Atkinson and Shiffrin (1968). Alcohol seems to influence most stages of the process to some degree, but its primary effect appears to be on the transfer of information from short-term to long-term storage. Intoxicated subjects are typically able to recall information immediately after it is presented and even keep it active in short-term memory for 1 minute or more if they are not distracted. Subjects also are normally able to recall long-term memories formed before they became intoxicated; however, beginning with just one or two drinks, subjects begin to show impairments in the ability to transfer information into long-term storage. Under some circumstances, alcohol can impact this process so severely that, once sober again, subjects are unable to recall critical elements of events, or even entire events, that occurred while they were intoxicated. These impairments are known as blackouts.

Figure 2

The human brain, showing the location of the hippocampus, the frontal lobes, and the medial septum.

Figure 3

Alcohol suppresses hippocampal pyramidal cell activity in an awake, freely behaving rat. Pyramidal cells often fire when the animal is in discrete regions of its environment, earning them the title “place-cells.” The specific areas of the environment where these cells fire are referred to as place-fields. The figure shows the activity of an individual pyramidal cell before alcohol administration (baseline), 45 to 60 minutes after alcohol administration, and 7 hours after alcohol administration (1.5 g/kg). Each frame in the figure shows the firing rate and firing location of the cell across a 15-minute block of time during which the rat was foraging for food on a symmetric, Y-shaped maze. White pixels are pixels in which the cell fired at very low rates, and darker colors represent higher firing rates (see key to the right of figure). As is clear from a comparison of activity during baseline and 45 to 60 minutes after alcohol administration, the activity of the cell was essentially shut off by alcohol. Neural activity returned to near normal levels within roughly 7 hours after alcohol administration.