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  • Journal List
  • Alcohol Res Health
  • v.27(ii); 2003
  • PMC6668891

Alcohol Res Health. 2003; 27(2): 186–196.

What Happened? Alcohol, Memory Blackouts, and the Brain

Abstract

Alcohol primarily interferes with the power to class new long-term memories, leaving intact previously established long-term memories and the ability to keep new data active in memory for brief periods. As the amount of alcohol consumed increases, so does the magnitude of the memory impairments. Large amounts of booze, especially if consumed speedily, 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 mutual 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 auotbiographical memories.

Keywords: alcoholic blackout, memory interference, AOD (alcohol and other drug) intoxication, AODE (booze and other drug furnishings), AODR (booze and other drug related) mental disorder, long-term memory, short-term retentiveness, country-dependent memory, BAC level, social AOD employ, drug interaction, affliction susceptibility, hippocampus, frontal cortex, neuroimaging, long-term potentiation

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 stated nearly 70 years ago, "the striking and inescapable impression one gets from a review of acute alcoholic intoxication is of the almost infinite multifariousness of symptoms that may ensue from the activity of this single toxic agent" (1935) (pp. 94–95). In addition to impairing balance, motor coordination, decisionmaking, and a litany of other functions, alcohol produces detectable memory impairments beginning after just 1 or ii drinks. Every bit the dose increases, so does the magnitude of the retentiveness impairments. Nether certain circumstances, alcohol can disrupt or completely block the power to form memories for events that transpire while a person is intoxicated, a type of damage known equally a blackout. This commodity reviews what is currently known regarding the specific features of acute alcohol-induced retentivity dysfunction, especially booze-induced blackouts, and the pharmacological mechanisms underlying them.

Effects of Alcohol on Memory

To evaluate the effects of alcohol, or any other drug, on retention, one must starting time identify a model of retention germination and storage to apply every bit a reference. One classic, often-cited model, initially proposed by Atkinson and Shiffrin (1968), posits that retention formation and storage accept identify in several stages, proceeding from sensory memory (which lasts up to a few seconds) to short-term retentivity (which lasts from seconds to minutes depending upon whether the information is rehearsed) to long-term storage. This model oft is referred to as the modal model of memory, as it captures central elements of several other major models. Indeed, elements of this model however tin can exist seen in nigh all models of memory germination.

In the modal model of memory, when i attends to sensory information, it is transferred from a sensory memory shop to brusk-term memory. The likelihood that information volition be transferred from short-term to long-term storage, or exist encoded into long-term memory, was once idea to depend primarily on how long the person keeps the data agile in short-term retention via rehearsal. Although rehearsal conspicuously influences the transfer of data into long-term storage, it is important to note that other factors, such equally the depth of processing (i.e., the level of true understanding and manipulation of the information), attention, motivation, and arousal besides play of import roles (Craik and Lockhart 1972; Otten et al. 2001; Eichenbaum 2002).1

Variability in the utilize of terms, particularly in operational definitions of curt-term retentivity, makes it difficult to codify a simple synopsis of the literature on alcohol-induced retentiveness impairments. As Mello (1973) stated three decades ago with regard to the memory literature in general, "The inconsistent utilize of descriptive terms has been a recurrent source of confusion in the 'brusque-term' memory literature and 'brusk-term' memory has been variously divers equally five seconds, 5 minutes, and thirty minutes" (p. 333). In spite of this inconsistency, several conclusions can exist drawn from research on alcohol-induced retentiveness impairments. Ane conclusion is that the impact of booze on the formation of new long-term "explicit" memories—that is, memories of facts (eastward.g., names and phone numbers) and events—is far greater than the drug's impact on the power to recollect previously established memories or to hold new information in short-term retentiveness (Lister et al. 1991). (See figure i for a diagram depicting the stages of memory and where alcohol interferes with retentiveness.) Intoxicated subjects are typically able to repeat new information immediately after its presentation and often can go on information technology active in brusk-term storage for up to a few minutes if they are not distracted (for an early on review, see Ryback 1971), though this is not always the case (Nordby et al. 1999). Similarly, subjects normally are capable of retrieving information placed in long-term storage prior to acute intoxication. In dissimilarity, alcohol impairs the power to store data across delays longer than a few seconds if subjects are distracted between the time they are given the new information and the time they are tested. In a classic study, Parker and colleagues (1976) reported that when intoxicated subjects were presented with "paired associates"—for instance, the letter "B" paired with the month "January"—they were dumb when asked to recall the items afterwards delays of a minute or more. Nevertheless, subjects could recall paired associates that they had learned before becoming intoxicated. More recently, Acheson and colleagues (1998) observed that intoxicated subjects could call up items on discussion lists immediately after the lists were presented just were impaired when asked to recall the items twenty minutes later.

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A full 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 almost stages of the process to some caste, simply its master effect appears to be on the transfer of information from short-term to long-term storage. Intoxicated subjects are typically able to recollect data immediately afterwards it is presented and even go along it active in short-term retentiveness for 1 infinitesimal or more if they are non distracted. Subjects likewise are normally able to recall long-term memories formed before they became intoxicated; however, beginning with just one or 2 drinks, subjects brainstorm 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 disquisitional elements of events, or even entire events, that occurred while they were intoxicated. These impairments are known as blackouts.

Ryback (1971) characterized the bear upon of booze on memory formation as a dose-related continuum, with small impairments at one end and large impairments at the other, all impairments representing the same fundamental deficit in the power to transfer new data from short-term to long-term storage. When doses of booze are small to moderate (producing blood alcohol concentrations [BACs] beneath 0.15 percent), retentiveness impairments tend to be small to moderate every bit well. At these levels, alcohol produces what Ryback (1971) referred to equally cocktail party memory deficits, lapses in memory that people might experience after having a few drinks at a cocktail party, often manifested as problems remembering what another person said or where they were in conversation. Several studies have revealed that alcohol at such levels causes difficulty forming memories for items on discussion lists or learning to recognize new faces (Westrick et al. 1988; Mintzer and Griffiths 2002). As the dose increases, the resulting memory impairments tin become much more than profound, sometimes culminating in blackouts—periods for which a person is unable to remember critical elements of events, or even unabridged events, that occurred while he or she was intoxicated.

Alcohol-Induced Blackouts

Blackouts correspond episodes of amnesia, during which subjects are capable of participating even in salient, emotionally charged events—likewise as more mundane events—that they afterward cannot remember (Goodwin 1995). Similar milder alcohol-induced memory impairments, these periods of amnesia are primarily "anterograde," meaning that booze impairs the power to form new memories while the person is intoxicated, but does not typically erase memories formed earlier intoxication. Formal research into the nature of alcohol-induced blackouts began in the 1940s with the work of E.1000. Jellinek (1946). Jellinek's initial characterization of blackouts was based on data collected from a survey of Alcoholics Bearding members. Noting that recovering alcoholics frequently reported having experienced alcohol-induced amnesia while they were drinking, Jellinek concluded that the occurrence of blackouts is a powerful indicator of alcoholism.

In 1969, Goodwin and colleagues published two of the virtually influential studies in the literature on blackouts (Goodwin et al. 1969a,b). Based on interviews with 100 hospitalized alcoholics, 64 of whom had a history of blackouts, the authors posited the existence of ii qualitatively different types of blackouts: en bloc and fragmentary blackouts. People experiencing en bloc blackouts are unable to recall whatever details any from events that occurred while they were intoxicated, despite all efforts by the drinkers or others to cue recall. Referring back to our general model of memory germination, it is as if the process of transferring information from short-term to long-term storage has been completely blocked. En bloc retention impairments tend to have a distinct onset. It is normally less clear when these blackouts cease considering people typically fall comatose before they are over. Interestingly, people announced able to keep information active in brusk-term retentivity for at least a few seconds. As a result, they tin oft carry on conversations, drive automobiles, and engage in other complicated behaviors. Information pertaining to these events is simply non transferred into long-term storage. Ryback (1970) wrote that intoxicated subjects in one of his studies "could carry on conversations during the amnesic state, but could non remember what they said or did v minutes earlier. Their firsthand and remote retentiveness were intact" (p. 1003). Similarly, in their study of memory impairments in intoxicated alcoholics, Goodwin and colleagues (1970) reported that subjects who experienced blackouts for testing sessions showed intact memory for up to two minutes while the sessions were taking identify.

Unlike en bloc blackouts, fragmentary blackouts involve partial blocking of memory formation for events that occurred while the person was intoxicated. Goodwin and colleagues (1969a) reported that subjects experiencing bitty blackouts often become aware that they are missing pieces of events only after being reminded that the events occurred. Interestingly, these reminders trigger at to the lowest degree some recall of the initially missing information. Enquiry suggests that fragmentary blackouts are far more common than those of the en bloc variety (White et al. 2004; Hartzler and Fromme 2003b; Goodwin et al. 1969b).

Blackouts: Land-Dependent Memory Formation?

Early anecdotal evidence suggested that blackouts might really reflect state-dependent data storage—that is, people might be able to recollect events that occurred while they were intoxicated if they returned to that country (e.chiliad., Goodwin et al. 1969a). State-dependent memory tin can exist viewed as a special instance of a broader category known as context-dependent memory (e.g., White et al. 2002a), in which cues that are associated with an upshot when a retentiveness is formed tend to help trigger recall for that consequence at a afterward time. For instance, in a classic study by Godden and Baddeley (1975) divers who learned word lists either on land or under h2o remembered more words when tested in the same context in which learning took place (i.east., land–land or water–h2o). Likewise, returning to the aforementioned emotional or physiological state that was nowadays when a memory was formed oft can facilitate call back of that memory. Information technology is non uncommon to hear stories of drinkers who stash alcohol or coin while intoxicated and can locate the hiding places only after becoming intoxicated again (Goodwin 1995). Regardless of how compelling such stories tin can exist, clear evidence of land-dependent learning under the influence of alcohol is lacking. In 1 recent study, Weissenborn and Duka (2000) examined whether subjects who learned give-and-take lists while intoxicated could think more items if they were intoxicated again during the testing session. No such state-dependency was observed. Similarly, Lisman (1974) tried unsuccessfully to assistance subjects resurrect lost information for events occurring during periods of intoxication by getting them intoxicated once again.

Blood Alcohol Concentrations and Blackouts

Drinking large quantities of alcohol oft precedes blackouts, just several other factors also appear to play of import roles in causing such episodes of memory loss. As Goodwin and colleagues (1969a) stated with regard to subjects in one of their studies, "Although blackouts well-nigh always were associated with heavy drinking, this lonely seemed insufficient to produce one. On many other occasions, subjects said they had drunk as much or more without memory loss" (p. 195). Amongst the factors that preceded blackouts were gulping drinks and drinking on an empty breadbasket, each of which leads to a rapid rising in BAC.

Subsequent enquiry provided additional evidence suggesting a link between blackouts and chop-chop rising BACs. Goodwin and colleagues (1970) examined the bear on of acute alcohol exposure on retention formation in a laboratory setting. The author recruited 10 male subjects for the project, all just ane through the unemployment role in St. Louis, Missouri. Most subjects met diagnostic criteria for alcoholism and one-half had a history of frequent blackouts. The men were asked to consume roughly xvi to xviii ounces of 86-proof bourbon in approximately 4 hours. Outset 1 hour after subjects began drinking, memory was tested by presenting subjects with several different stimuli, including a series of children's toys and scenes from erotic films. Subjects were asked to retrieve details regarding these stimuli ii minutes, 30 minutes, and 24 hours after the stimuli were shown. One-half of the subjects reported no think for the stimuli or their presentation 30 minutes and 24 hours later the events, though most seemed to think the stimuli 2 minutes after presentation. Lack of call up for the events 24 hours later, while sober, represents articulate experimental bear witness for the occurrence of blackouts. The fact that subjects could remember aspects of the events 2 minutes after they occurred but not 30 minutes or 24 hours afterward provides compelling evidence that the blackouts stemmed from an inability to transfer information from brusk-term to long-term storage. For all just one subject in the coma grouping, retentiveness impairments began during the beginning few hours of drinking, when BAC levels were still ascent. The average peak BAC in this grouping, which was roughly 0.28 pct, occurred approximately two.v hours after the onset of drinking.

In a like study, Ryback (1970) examined the touch of alcohol on memory in seven hospitalized alcoholics given access to alcohol over the grade of several days. All subjects were White males betwixt the ages of 31 and 44. Blackouts occurred in 5 of the vii subjects, as evidenced by an inability to recall salient events that occurred while drinking the day earlier (eastward.g., one subject could not recall preparing to hit another over the caput with a chair). Estimates of BAC levels during blackout periods suggested that they often began at levels around 0.20 per centum and equally low every bit 0.14 percentage. The duration of blackouts ranged from 9 hours to three days. Based on his observations, Ryback concluded that a key predictor of blackouts was the charge per unit at which subjects consumed their drinks. He stated, "It is important to note that all the blackout periods occurred afterwards a rapid rising in claret alcohol level" (p. 622). The 2 subjects who did not black out, despite becoming extremely intoxicated, experienced slow increases in blood booze levels.

Blackouts Amongst Social Drinkers

Most of the research conducted on blackouts during the by fifty years has involved surveys, interviews, and direct ascertainment of middle-anile, primarily male person alcoholics, many of whom were hospitalized. Researchers have largely ignored the occurrence of blackouts among young social drinkers, and then the idea that blackouts are an unlikely consequence of heavy drinking in nonalcoholics has remained securely entrenched in both the scientific and pop cultures. Withal at that place is clear testify that blackouts do occur amid social drinkers. Knight and colleagues (1999) observed that 35 percent of trainees in a large pediatric residency program had experienced at least one blackout. Similarly, Goodwin (1995) reported that 33 percent of the first-yr medical students he interviewed best-selling having had at least 1 blackout. "They were inexperienced," he wrote. "They drank too much too quickly, their blood levels rose extremely quickly, and they experienced amnesia" (p. 315). In a study of 2,076 Finnish males, Poikolainen (1982) plant that 35 percent of all males surveyed had had at least one coma in the year before the survey.

As might exist expected given the excessive drinking habits of many college students (Wechsler et al. 2002), this population commonly experiences blackouts. White and colleagues (2002c) recently surveyed 772 undergraduates regarding their experiences with blackouts. Respondents who answered aye to the question "Have y'all ever awoken after a night of drinking not able to remember things that y'all did or places that you went?" were considered to have experienced blackouts. L-one percent of the students who had always consumed alcohol reported blacking out at some signal in their lives, and 40 percent reported experiencing a blackout in the year before the survey. Of those who had consumed alcohol during the two weeks earlier the survey, 9.four percent reported blacking out during this period. Students in the study reported that they afterward learned that they had participated in a wide range of events they did not remember, including such significant activities as vandalism, unprotected intercourse, driving an motorcar, and spending money.

During the ii weeks preceding the survey, an equal pct of males and females experienced blackouts, despite the fact that males drank significantly more often and more heavily than females. This outcome suggests that at any given level of alcohol consumption, females—a group infrequently studied in the literature on blackouts—are at greater risk than males for experiencing blackouts. The greater tendency of females to blackness out likely arises, in part, from well-known gender differences in physiological factors that affect booze distribution and metabolism, such every bit body weight, proportion of body fatty, and levels of key enzymes. There likewise is some testify that females are more susceptible than males to milder forms of booze-induced retentiveness impairments, even when given comparable doses of alcohol (Mumenthaler et al. 1999).

In a subsequent study, White and colleagues (2004) interviewed 50 undergraduate students, all of whom had experienced at least one coma, to gather more information about the factors related to blackouts. As in the previous report, students reported engaging in a range of risky behaviors during blackouts, including sexual action with both acquaintances and strangers, vandalism, getting into arguments and fights, and others. During the night of their most contempo blackout, most students drank either liquor alone or in combination with beer. Only 1 student out of 50 reported that the about recent blackout occurred after drinking beer solitary. On boilerplate, students estimated that they consumed roughly 11.5 drinks earlier the onset of the blackout. Males reported drinking significantly more than females, but they did and so over a significantly longer period of fourth dimension. As a result, estimated peak BACs during the night of the last blackout were similar for males (0.30 pct) and females (0.35 percent). As Goodwin observed in his piece of work with alcoholics (1969b), fragmentary blackouts occurred far more often than en bloc blackouts, with four out of five students indicating that they eventually recalled bits and pieces of the events. Roughly half of all students (52 percent) indicated that their first full memory after the onset of the coma was of waking upwards in the morning, often in an unfamiliar location. Many students, more females (59 percent) than males (25 percent), were frightened by their last coma and changed their drinking habits equally a consequence.

Apply of Other Drugs During Blackouts

Alcohol interacts with several other drugs, many of which are capable of producing amnesia on their ain. For instance, diazepam (Valium®) and flunitrazepam (Rohypnol) are benzodiazepine sedatives that can produce astringent memory impairments at loftier doses (White et al. 1997; Saum and Inciardia 1997). Alcohol enhances the effects of benzodiazepines (for a review, see Silvers et al. 2003). Thus, combining these compounds with alcohol could dramatically increment the likelihood of experiencing memory impairments. Similarly, the combination of alcohol and THC, the primary psychoactive compound in marijuana, produces greater memory impairments than when either drug is given solitary (Ciccocioppo et al. 2002). Given that many higher students use other drugs in combination with alcohol (O'Malley and Johnston 2002), some of the blackouts reported by students may arise from polysubstance use rather than from alcohol solitary. Indeed, based on interviews with 136 heavy-drinking young adults (hateful age 22), Hartzler and Fromme (2003b) ended that en bloc blackouts oftentimes arise from the combined utilize of booze and other drugs. White and colleagues (2004) observed that, among l undergraduate students with a history of blackouts, but 3 students reported using other drugs during the night of their most contempo blackout, and marijuana was the drug in each instance.

Are Some People More Likely Than Others to Experience Blackouts?

In classic studies of hospitalized alcoholics by Goodwin and colleagues (1969a,b), 36 out of the 100 patients interviewed indicated that they had never experienced a blackout. In some means, the patients who did not feel blackouts are every bit interesting as the patients who did. What was information technology near these 36 patients that kept them from blacking out, despite the fact that their alcoholism was so severe that it required hospitalization? Although they may actually have experienced blackouts just just were unaware of them, in that location may take been something fundamentally dissimilar near these patients that diminished their likelihood of experiencing memory impairments while drinking.

In back up of this possibility, a recent written report by Hartzler and Fromme (2003a) suggests that people with a history of blackouts are more vulnerable to the effects of booze on memory than those without a history of blackouts. These authors recruited 108 college students, half of whom had experienced at least one fragmentary blackout in the previous twelvemonth. While sober, members of the two groups performed comparably in retention tasks. Withal, when they were mildly intoxicated (0.08 per centum BAC) those with a history of fragmentary blackouts performed worse than those without such a history. At that place are two possible interpretations for these data, both of which support the hypothesis that some people are more than susceptible to blackouts than others. Ane plausible interpretation is that subjects in the bitty blackout grouping always have been more than vulnerable to booze-induced memory impairments, which is why they performed poorly during testing under alcohol, and why they are members of the blackout grouping in the first place. A 2nd estimation is that subjects in the blackout group performed poorly during testing as a result of drinking plenty in the past to experience booze-induced retention impairments. In other words, perhaps their prior exposure to alcohol damaged the encephalon in a way that predisposed them to experiencing future retentivity impairments. This latter possibility is fabricated more than likely by recent evidence that students who engage in repeated episodes of heavy, or binge, drinking are more likely than other students to showroom memory impairments when they are intoxicated (Weissenborn and Duka 2000). Like results accept been observed in creature studies (White et al. 2000a).

The argument for an inherent vulnerability to alcohol-induced memory impairments, including blackouts, is strengthened past two recent studies. In an impressive longitudinal written report, Baer and colleagues (2003) examined the drinking habits of pregnant women in 1974 and 1975, and and then studied alcohol utilise and related issues in their offspring at vii different time points during the post-obit 21 years. These authors observed that prenatal alcohol exposure was associated with increased rates of experiencing booze-related consequences, including blackouts, fifty-fifty after controlling for the offsprings' general drinking habits. In addition, a recent report past Nelson and colleagues (2004) suggests that there might actually be a genetic contribution to the susceptibility to blackouts, indicating that some people only are congenital in a way that makes them more vulnerable to booze-induced amnesia.

As discussed in the department below on the potential encephalon mechanisms underlying alcohol-induced amnesia, it is like shooting fish in a barrel to imagine that the impact of alcohol on brain circuitry could vary from person to person, rendering some people more than sensitive than others to the memory-impairing effects of the drug.

How Does Alcohol Impair Memory?

During the beginning half of the 20th century, two theoretical hurdles hampered progress toward an agreement of the mechanisms underlying the effects of booze on memory. More contempo research has cleared abroad these hurdles, allowing for tremendous gains in the area during the past 50 years.

The first hurdle concerned scientists' understanding of the functional neuroanatomy of memory. In the 1950s, following observations of an amnesic patient known as H.1000., it became clear that unlike brain regions are involved in the formation, storage, and retrieval of unlike types of retentivity. In 1953, large portions of H.M.'south medial temporal lobes, including most of his hippocampus, were removed in an effort to control intractable seizures (Scoville and Milner 1957). Although the frequency and severity of H.M.'s seizures were significantly reduced past the surgery, information technology soon became clear that H.M. suffered from a dramatic syndrome of retentivity impairments. He even so was able to learn basic motor skills, continue information active in short-term retentiveness for a few seconds or more if left undistracted, and remember episodes of his life from long ago, but he was unable to form new long-term memories for facts and events. The design of H.One thousand.'south impairments besides forced a re-exam of models of long-term retentiveness storage. Specifically, although H.M. was able to retrieve long-term memories formed roughly a year or more before his surgery, he could not recall events that transpired inside the year preceding his surgery. This strongly suggests that the transfer of data into long-term storage actually takes place over several years, with the hippocampus being necessary for its retrieval for the first yr or so.

Subsequent research with other patients confirmed that the hippocampus, an irregularly shaped structure deep in the forebrain, is critically involved in the germination of memories for events (run into figure 2 for a depiction of the brain, with the hippocampus and other relevant structures highlighted). Patient R.B. lost a significant amount of blood every bit a result of heart surgery. He survived but showed memory impairments similar to those exhibited by H.M. Upon his death, histology revealed that the loss of blood to R.B.'s brain damaged a pocket-sized region of the hippocampus called hippocampal surface area CA1, which contains neurons known as pyramidal cells because of the triangular shape of their cell bodies (Zola-Morgan et al. 1986). Hippocampal CA1 pyramidal cells assistance the hippocampus in communicating with other areas of the encephalon. The hippocampus receives information from a wide variety of brain regions, many of them located in the tissue, called the neocortex, that blankets the brain and surrounds other encephalon structures. (Neocortex literally means "new bawl" or "new roofing." When ane looks at a picture of the human encephalon, most of what is visible is neocortex.) The hippocampus somehow ties data from other brain regions together to course new autobiographical memories, and CA1 pyramidal cells send the results of this processing back out to the neocortex. As is articulate from patient R.B., removing CA1 pyramidal cells from the circuitry prevents the hippocampal memory organisation from doing its job.

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

The second barrier to understanding the mechanisms underlying alcohol'southward effects on memory was an incomplete agreement of how booze affects brain function at a cellular level. Until recently, booze was assumed to touch the brain in a general manner, simply shutting down the action of all cells with which information technology came in contact. The pervasiveness of this assumption is reflected in numerous writings during the early 20th century. For example, Fleming (1935) wrote, "The prophetic generalization of Schmiedeberg in 1833 that the pharmacological activity of alcohol on the cerebrum is purely depressant has been constitute, well-nigh pharmacologists volition agree, to characterize its action in full general on all tissues" (p. 89). During the 1970s, researchers hypothesized that alcohol depressed neural activity by altering the movement of key molecules (in particular, lipids) in nerve jail cell membranes. This change then led to alterations in the activity of proteins, including those that influence communication between neurons by controlling the passage of positively or negatively charged atoms (i.e., ions) through cell membranes (e.thousand., Mentum and Goldstein 1977). This view persisted into the tardily 1980s, at which time the consensus began to shift as bear witness mounted that alcohol has selective effects on the brain's nerve-cell communication (i.east., neurotransmitter) systems, altering activeness in some types of receptors only not others (e.g., Criswell et al. 1993). Substantial evidence now indicates that alcohol selectively alters the activeness of specific complexes of proteins embedded in the membranes of cells (i.e., receptors) that demark neurotransmitters such as gamma-aminobutyric acrid (GABA), glutamate, serotonin, acetylcholine, and glycine (for a review, encounter Piddling 1999). In some cases, merely a few amino acids appear to distinguish receptors that are sensitive to alcohol from those that are non (Peoples and Stewart 2000). Information technology remains unclear exactly how alcohol interacts with receptors to alter their activity.

Alcohol, Retention, and the Hippocampus

More than 30 years ago, both Ryback (1970) and Goodwin and colleagues (1969a) speculated that alcohol might impair memory formation by disrupting activity in the hippocampus. This speculation was based on the observation that acute alcohol exposure (in humans) produces a syndrome of memory impairments similar in many ways to the impairments produced by hippocampal impairment. Specifically, both acute alcohol exposure and hippocampal harm impair the ability to class new long-term, explicit memories but practise non affect short-term memory storage or, in general, the recall of information from long-term storage.

Research conducted in the past few decades using creature models supports the hypothesis that alcohol impairs memory germination, at least in office, by disrupting activity in the hippocampus (for a review, see White et al. 2000b). Such research has included behavioral ascertainment; examination of slices of and brain tissue, neurons in cell culture, and brain action in anesthetized or freely behaving animals; and a multifariousness of pharmacological techniques.

As mentioned above, damage express to the CA1 region of the hippocampus dramatically disrupts the ability to class new explicit memories (Zola-Morgan et al. 1986). In rodents, the actions of CA1 pyramidal cells have striking behavioral correlates. Some cells tend to discharge electrical signals that upshot in one cell communicating with other cells (i.e., activeness potentials) when the rodent is in a distinct location in its environment. The location differs for each cell. For instance, while a rat searches for food on a plus-shaped maze, one pyramidal cell might generate activeness potentials primarily when the rat is at the far cease of the north arm, while another might generate action potentials primarily when the rat is in the middle of the s arm, and and then on. Collectively, the cells that are active in that particular environment create a spatial, or contextual map that serves as a framework for issue memories created in that environment. Because of the location-specific firing of these cells, they often are referred to equally "place-cells," and the regions of the environment in which they fire are referred to as "place-fields" (for reviews, see Best and White 1998; Best et al. 2001). Given that CA1 pyramidal cells are critically of import to the formation of memories for facts and events, and the articulate behavioral correlates of their action in rodents, information technology is possible to assess the bear on of alcohol on hippocampal output in an intact, fully functional brain by studying these cells.

In contempo work with awake, freely behaving rats, White and All-time (2000) showed that alcohol profoundly suppresses the activity of pyramidal cells in region CA1. The researchers allowed the rats to forage for food for 15 minutes in a symmetric, Y-shaped maze and measured the animals' hippocampal activity using tiny wires (i.eastward., microelectrodes) implanted in their brains. Figure iii displays the activity of an private CA1 pyramidal prison cell. The activity—which corresponds to the middle portion of the lower left arm of the maze—is shown earlier alcohol administration (A), 45 to threescore minutes after alcohol administration (B), and 7 hours subsequently alcohol administration (C). The dose of booze used in the testing session was 1.5 grams per kilogram of body weight— plenty to produce a elevation BAC of about 0.16 percent. (A corresponding BAC in humans would exist twice the legal driving limit in most States.) As the figure illustrates, the prison cell's activity was substantially shut off by alcohol. Neural activity returned to near-normal levels within nearly 7 hours of booze administration.

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Alcohol suppresses hippocampal pyramidal cell activeness in an awake, freely behaving rat. Pyramidal cells often burn when the brute is in discrete regions of its environment, earning them the championship "place-cells." The specific areas of the environment where these cells fire are referred to every bit place-fields. The figure shows the action of an private pyramidal prison 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 effigy shows the firing rate and firing location of the jail cell beyond 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). Equally is clear from a comparison of activity during baseline and 45 to sixty minutes afterward alcohol administration, the activeness of the cell was essentially shut off past alcohol. Neural activity returned to most normal levels within roughly 7 hours after alcohol administration.

White and Best administered several doses of alcohol in this study, ranging from 0.5 g/kg to one.5 yard/kg. (Only one of the experiments is represented in figure 3.) They plant that the dose affected the degree of pyramidal prison cell suppression. Although 0.5 g/kg did non produce a significant change in the firing of hippocampal pyramidal cells, 1.0 and 1.5 k/kg produced meaning suppression of firing during a ane-hour testing session post-obit booze assistants. The dose-dependent suppression of CA1 pyramidal cells is consistent with the dose-dependent effects of booze on episodic retention formation.

Alcohol and Hippocampal Long-Term Potentiation

In add-on to suppressing the output from pyramidal cells, alcohol has several other effects on hippocampal role. For case, alcohol severely disrupts the ability of neurons to establish long-lasting, heightened responsiveness to signals from other cells (Bliss and Collinridge 1993). This heightened responsiveness is known as long-term potentiation (LTP). Considering researchers have theorized that something similar LTP occurs naturally in the brain during learning (for a review, come across Martin and Morris 2002), many investigators have used LTP every bit a model for studying the neurobiology underlying the effects of drugs, including alcohol, on memory.

In a typical LTP experiment, 2 electrodes (A and B) are lowered into a slice of hippocampal tissue kept alive by bathing information technology in oxygenated artificial cerebral spinal fluid (ACSF). A small amount of electric current is passed through electrode A, causing the neurons in this surface area to send signals to cells located about electrode B. Electrode B then is used to record how the cells in the area reply to the incoming signals. This response is the baseline response. Side by side, a specific pattern of stimulation intended to model the blueprint of activity that might occur during an actual learning upshot is delivered through electrode A. When the original stimulus that elicited the baseline response is delivered again through electrode A, the response recorded at electrode B is larger (i.e., potentiated). In other words, every bit a result of the patterned input, cells at position B now are more responsive to signals sent from cells at position A. The potentiated response frequently lasts for an extended flow of time, hence the term long-term potentiation.

Alcohol interferes with the establishment of LTP (Morrisett and Swartzwelder 1993; Givens and McMahon 1995; Pyapali et al. 1999; Schummers and Browning 2001), and this damage begins at concentrations equivalent to those produced past consuming just one or two standard drinks (e.g., a 12-oz beer, 1.5-oz of liquor in a shot or mixed drink, or a 5-oz glass of wine) (Blitzer et al. 1990). If sufficient alcohol is present in the ACSF bathing the slice of hippocampal tissue when the patterned stimulation is given, the response recorded afterwards at position B volition non be larger than it was at baseline (that is, it will non be potentiated). And, only every bit alcohol tends not to impair think of memories established before alcohol exposure, alcohol does not disrupt the expression of LTP established before booze exposure.

One of the key requirements for the establishment of LTP in the hippocampus is that a type of betoken receptor known every bit the NMDAtwo receptor becomes activated. Activation of the NMDA receptor allows calcium to enter the jail cell, which sets off a chain of events leading to long-lasting changes in the cell's structure or role, or both. Alcohol interferes with the activation of the NMDA receptor, thereby preventing the influx of calcium and the changes that follow (Swartzwelder et al. 1995). This is believed to be the chief machinery underlying the effects of booze on LTP, though other transmitter systems probably are also involved (Schummers and Browning 2001).

Indirect Effects of Alcohol on Hippocampal Function

Similar other encephalon regions, the hippocampus does not operate in isolation. Information processing in the hippocampus depends on coordinated input from a multifariousness of other structures, which gives booze and other drugs boosted opportunities to disrupt hippocampal functioning. One encephalon region that is primal to hippocampal functioning is a minor structure in the fore brain known as the medial septum (Givens et al. 2000). The medial septum sends rhythmic excitatory and inhibitory signals to the hippocampus, causing rhythmic changes in the activity of hippocampal pyramidal cells. In electroencephalograph recordings, this rhythmic activeness, referred to as the theta rhythm, occurs within a frequency of roughly 6 to 9 cycles per second (hertz) in actively behaving rats. The theta rhythm is idea to act as a gatekeeper, increasing or decreasing the likelihood that information entering the hippocampus from cortical structures volition be candy (Orr et al. 2001). (For more information on the function of electrophysiology in diagnosing alcohol issues, encounter the commodity in this outcome by Porjesz and Begleiter.) Information inbound the hippocampus when pyramidal cells are slightly excited (i.e., slightly depolarized) has a better chance of influencing hippocampal circuitry than signals that arrive when the cells are slightly suppressed (i.e., slightly hyperpolarized).

Manipulations that disrupt the theta rhythm also disrupt the power to perform tasks that depend on the hippocampus (Givens et al. 2000). Booze disrupts the theta rhythm in big role by suppressing the output of signals from medial septal neurons to the hippocampus (Steffensen et al. 1993; Givens et al. 2000). Given the powerful influence that the medial septum has on information processing in the hippocampus, the impact of alcohol on cellular activeness in the medial septum is probable to play an important role in the effects of alcohol on retentiveness. Indeed, in rats, putting alcohol directly into the medial septum alone produces memory impairments (Givens and McMahon 1997).

Other Brain Regions Involved in Alcohol-Induced Retention Impairments

The hippocampus is non the only structure involved in retention formation. A host of other brain structures also are involved in memory formation, storage, and retrieval (Eichenbaum 2002). Recent research with humans has yielded compelling show that key areas of the frontal lobes play of import roles in brusk-term retention 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 operation of the other.

Considerable prove suggests that chronic booze utilize 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 encephalon volume, changes in factor expression, and disruptions in how performing sure tasks affects blood flow in the encephalon all have been observed in the frontal lobes of booze-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 furnishings of chronic (i.e., repeated) use of alcohol on frontal lobe part, little is known about the furnishings of one-fourth dimension (i.e., acute) use of alcohol on activeness in the frontal lobes, or the human relationship of such effects to alcohol-induced memory impairments. Compelling show indicates that acute alcohol use impairs the functioning of a variety of frontal lobe–mediated tasks, similar those that require planning, decisionmaking, and impulse control (Weissenborn and Duka 2003; Burian et al. 2003), simply the underlying mechanisms are not known. Research likewise suggests that baseline claret 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 corporeality of activeness that occurs in the frontal lobes when the frontal lobes are exposed to pulses from a strong magnetic field (Kahkonen et al. 2003). Although the exact meaning of these changes remains unclear, the testify suggests that acute intoxication alters the normal functioning of the frontal lobes. Future research is needed to shed more calorie-free on this of import question. In item, inquiry in animals will exist an important supplement to studies in humans, affording a better agreement of the underlying prefrontal circuitry involved in alcohol-induced retentiveness damage.

Summary and Conclusions

As detailed in this brief review, alcohol can have a dramatic impact on memory. Alcohol primarily disrupts the ability to course new long-term memories; it causes less disruption of recall of previously established long-term memories or of the power to keep new information agile in short-term retention for a few seconds or more. At low doses, the impairments produced past booze are frequently subtle, though they are detectable in controlled weather condition. As the amount of booze consumed increases, so does the magnitude of the memory impairments. Large quantities of alcohol, particularly if consumed speedily, tin produce a blackout, an interval of fourth dimension for which the intoxicated person cannot recall key details of events, or even unabridged events. En bloc blackouts are stretches of fourth dimension for which the person has no retention whatsoever. Fragmentary blackouts are episodes for which the drinker'southward retention is spotty, with "islands" of memory providing some insight into what transpired, and for which more recollect usually is possible if the drinker is cued by others. Blackouts are much more common among social drinkers than previously assumed and should exist viewed as a potential event of acute intoxication regardless of age or whether one is clinically dependent upon alcohol.

Tremendous progress has been made toward an understanding of the mechanisms underlying alcohol-induced retentiveness impairments. Alcohol disrupts activity in the hippocampus via several routes—directly, through effects on hippocampal circuitry, and indirectly, by interfering with interactions between the hippocampus and other brain regions. The touch of alcohol on the frontal lobes remains poorly understood, but probably plays an of import role in alcohol-induced memory impairments.

Modern neuroimaging techniques, such as positron emission tomography (PET) and functional magnetic resonance imaging (fMRI), provide incredible opportunities for investigating the bear upon of drugs like booze on encephalon function during the performance of cognitive tasks. The use of these techniques will no doubt yield important information regarding the mechanisms underlying alcohol-induced memory impairments in the coming years. Memory formation and retrieval are highly influenced past factors such as attending and motivation (eastward.g., Kensinger et al. 2003). With the aid of neuroimaging techniques, researchers may be able to examine the impact of alcohol on encephalon activity related to these factors, and then make up one's mind how alcohol contributes to retentivity impairments.

Despite advances in human neuroimaging techniques, fauna models remain absolutely essential in the study of mechanisms underlying alcohol-induced memory impairments. Hopefully, futurity work will reveal more than regarding the ways in which the effects of alcohol on multiple transmitter systems interact to disrupt memory formation. Similarly, recent advances in electrophysiological recording techniques, which permit for recordings from hundreds of private cells in several brain regions simultaneously (Kralik et al. 2001), could provide much-needed data regarding the impact of alcohol on the interactions between disparate brain regions involved in the encoding, storage, and retrieval of information.

Footnotes

1It is well beyond the scope of this review to assess the impact of alcohol on memory utilizing multiple perspectives on information processing and storage. For simplicity, this review will characterize the effects of alcohol on retention using a three-stage process of memory formation akin to the modal model. The interpretation of the effects of alcohol on memory probable would vary somewhat depending on the memory model ane uses.

2 N-methyl-D-aspartate (NMDA) is a receptor for the neurotransmitter glutamate.

This work was supported by National Institute on Alcohol Corruption and Alcoholism grant AA–12478 and the Found for Medical Research at the VA Medical Center in Durham, N Carolina.

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