What Are Blackouts? – Alcohol-related blackouts are gaps in a person’s memory for events that occurred while they were intoxicated. These gaps happen when a person drinks enough alcohol to temporarily block the transfer of memories from short-term to long-term storage—known as memory consolidation—in a brain area called the hippocampus.
- 0.1 The MOST SHOCKING Hells Angels SEX Rules – Exposed By Undercover Agent
- 1 What causes a person to blackout?
- 2 Why do I blackout after 2 drinks?
- 3 Can I drink without getting drunk?
- 4 How do you pass out drunk?
- 5 Is blacking out an emergency?
- 6 Can anxiety cause blackouts?
- 7 What happens when you drink too much alcohol at once?
What happens when you blackout from drinking?
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.
The MOST SHOCKING Hells Angels SEX Rules – Exposed By Undercover Agent
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 (alcohol and other drug effects), AODR (alcohol and other drug related) mental disorder, long-term memory, short-term memory, state-dependent memory, BAC level, social AOD use, drug interaction, disease 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 diversity of symptoms that may ensue from the action 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 one or two drinks. As the dose increases, so does the magnitude of the memory impairments.
What causes a person to blackout?
Blackouts & Fainting Symptoms | Heart Health Most unexplained blackouts are caused by syncope Many people, including doctors, assume that blackouts are due to epileptic seizures, but much more commonly they are due to syncope (pronounced sin-co-pee) – a type of blackout which is caused by a problem in the regulation of or sometimes with the heart.
Up to 40% of the population will lose consciousness at some point in their life due to syncope. Syncope can affect all age groups but the causes vary with age, and in older adults multiple causes often exist. Many syncopal attacks only require reassurance from your GP Many syncopal attacks require only explanation and reassurance from a GP or trained nurse regarding the likely absence of anything being seriously wrong.
Consultation with a specialist will be necessary, though, if the cause of the syncope remains uncertain or if there are particularly concerning symptoms or there is a family history of a heart condition. There are three major reasons for why people may experience a blackout(s):
Syncope: a sudden lack of blood supply to the brain. Syncope is caused by a problem in the regulation of blood pressure or by a problem with the heart. : an electrical ‘short-circuiting’ in the brain. Epileptic attacks are usually called seizures. Diagnosis of epilepsy is made by a, Psychogenic blackouts: resulting from stress or anxiety. Psychogenic blackouts occur most often in young adults. They may be very difficult to diagnose. ‘Psychogenic’ does not mean that people are ‘putting it on’. However there is often underlying stress due to extreme pressure at school or work. In exceptional cases it may be that some people have experienced ill treatment or abuse in childhood.
Misdiagnosis is common but avoidable:
Many syncopal attacks are mistaken for epilepsy.However epilepsy only affects slightly less than 1% of the population.UK research has shown that approximately 30% of adults and up to 40% of children diagnosed with epilepsy in the UK do not have the condition.Many elements of a syncopal attack, such as random jerking of limbs, are similar to those experienced during an epileptic seizure.It can be difficult to tell the causes of the blackout apart.
Syncope causes falls:
Syncope causes a significant number of falls in older adults, particularly where the falls are sudden and not obviously the result of a trip or slip.Many older adults will only recall a fall and will not realise they have blacked out.Greater awareness of syncope as a cause of falls is key to effective treatment and prevention of recurring falls.
: Blackouts & Fainting Symptoms | Heart Health
How can I drink without blacking out?
Download Article Download Article Getting tipsy from time to time can be fun, but it can quickly turn scary if you wake up the next day with little or no memory of what happened the night before. “Blackout” is the term for memory loss or impairment that happens when you drink.
It’s not the same as passing out or losing consciousness—you might even behave and converse fairly normally when you’re blackout drunk, but simply fail to recall much of what you did or said once you sober up. While blackouts can happen to anyone, you can reduce the risk by taking precautions such as pacing yourself and never drinking on an empty stomach.
If you frequently drink to the point of blacking out, or if you have other concerns about your drinking habits, talk to your doctor.
- 1 Drink slowly to prevent a rapid rise in blood-alcohol concentration (BAC). A sudden spike in the amount of alcohol in your blood is one of the biggest risk factors for a blackout. To avoid blacking out, pace yourself when you drink. Avoid gulping down your drink or having several drinks in a row without taking breaks in between.
- Drink a “spacer” between alcoholic beverages, such as a glass of soda, some juice, or even a non-alcoholic beer.
- Take small sips and make a conscious effort to savor your drink.
- Set your glass down after every sip.
- Avoid topping off your glass—don’t refill it until it’s empty.
- 2 Limit yourself to no more than 1-2 drinks per day. You’re more likely to have blackouts if you binge drink—that is, have several drinks within a relatively short period of time. Avoid binges by limiting your intake to no more than 1 drink per day if you’re a woman or 2 drinks if you’re a man.
- 1 drink is defined as 12 fluid ounces (350 mL) of beer (5% alcohol), 5 fluid ounces (150 mL) of wine (12% alcohol), or 1.5 fluid ounces (44 mL) of 80 proof distilled spirits (40% alcohol).
- Binge drinking is technically defined as any level of drinking that causes you to reach a BAC of 0.08% or higher. For most people, this happens after having 4-5 drinks within a 2-hour period. However, everyone reacts to alcohol differently, so your personal tolerance level may be higher or lower.
- 3 Stick to drinks with a lower alcohol content. The higher the alcohol content in a beverage, the more likely it is to make you blackout drunk. Avoid sending your BAC through the roof by sticking to drinks like beer or cider rather than hard liquors.
- If you want to drink something harder, mix it with a generous amount of a non-alcoholic mixer, such as tonic water, soda, or juice.
- Avoid mixed drinks, since mixing multiple types of alcohol will cause you to take in a lot more alcohol in a shorter period of time.
- 4 Consume food and water along with alcoholic drinks. Never drink on an empty stomach, since doing so will cause your body to absorb alcohol much faster. You’re less likely to get blackout drunk if you drink alcohol with a meal. Drinking plenty of water will also help slow the absorption of alcohol.
- In addition to slowing down the effects of alcohol, filling up on food and water may help you feel fuller so that you’re not tempted to drink as much.
- 5 Avoid drinking alcohol while taking other drugs or medications. Certain medications or drugs can interact with alcohol, making it more likely for you to experience blackouts or other unwanted side effects. Read all your medication labels carefully or talk to your doctor or pharmacist about whether you can safely use them in combination with alcohol.
- Medications that reduce anxiety and promote sleep, such as benzodiazepines, are especially likely to cause blackouts when combined with alcohol.
- Taking alcohol and antidepressants together can make your depression worse, increase the effects of the alcohol, and make you more prone to side effects like drowsiness and dizziness.
- Don’t mix alcohol with other recreational drugs, since this can also have dangerous or unexpected side effects.
- 6 Have a designated non-drinker with you if you’re blackout-prone. Blackouts can put you at greater risk of ending up in dangerous situations or behaving in risky or inappropriate ways. If you know you tend to black out while drinking, try to drink with a friend who’s willing to stay sober and help keep you out of trouble.
- Ask your friend to remind you to pace yourself. Try saying something like, “Hey, if you see me drinking too much at the party tonight, can you tell me to take a break and grab a snack?”
- 7 Cut back or abstain from drinking if you have alcoholic relatives. If alcoholism runs in your family, you’re more likely to be at risk of frequent blackouts. Take extra care to drink in moderation or avoid drinking altogether if you have one or more relatives with a drinking problem. Did you know? Although having a family history of alcoholism puts you at greater risk, blackouts aren’t necessarily a sign of alcoholism. Anybody can have a blackout while drinking alcohol, regardless of your level of drinking experience.
- 1 See your doctor if you have concerns about your drinking habits. If you have frequent blackouts, are concerned that you drink too much, or have questions about how alcohol might be affecting your health, talk to your doctor. They can work with you to help determine whether you might have a drinking problem. It’s a good idea to see your doctor if:
- You’re worried about how much you drink.
- Your drinking is interfering with your daily life, work, or relationships.
- Your friends or family have started expressing concern about your drinking habits.
- You drink even in situations where it might put you or others at risk, such as before driving or operating heavy machinery.
- You’ve tried to quit or cut back multiple times without success.
- You experience frequent blackouts or other negative effects from drinking, like vomiting, hangovers, or withdrawal symptoms.
- 2 Discuss possible treatment options if you’re alcohol dependent. If you’re struggling to quit or cut back on your alcohol intake, there are a variety of treatments that can help. Ask your doctor to recommend behavioral strategies to help you quit, or talk about other treatment options, such as:
- A medically supervised detox program to help you manage withdrawal symptoms.
- Psychological therapy to help you develop a recovery plan, learn appropriate coping skills, and deal with underlying conditions that might contribute to your drinking habits.
- Medications to help reduce your craving for alcohol or block the enjoyable effects of drinking.
Warning: Quitting cold turkey is difficult for most people, and it could even be dangerous if you have a severe alcohol dependency. Talk to your doctor about developing a plan to stop drinking gradually and safely.
- 3 Get emergency medical care if you suspect alcohol poisoning, Drinking too much, too fast can put you at risk of developing alcohol poisoning. This condition can be life-threatening, so it’s important to seek help immediately if it happens. Call emergency services if you suspect that someone you know has alcohol poisoning, and stay with them until help arrives.
- Symptoms of alcohol poisoning include severe confusion, vomiting, seizures, slow or irregular breathing, skin that is cold, pale, or blue-tinged, and loss of consciousness.
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Due to differences in anatomy and body chemistry, women and people who were assigned female at birth are typically more sensitive to alcohol than men or people who were assigned male at birth. This means that you may be at greater risk of blackouts from a relatively small amount of alcohol if you’re female or AFAB.
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What does it mean to black out?
: to undergo a temporary loss of vision, consciousness, or memory (as from temporary impairment of cerebral circulation, retinal anoxia, a traumatic emotional blow, or an alcoholic binge) compare gray out, red out. transitive verb. : to cause to black out.
Is blacking out bad for the brain?
Alcohol Rehab At Healthy Life Recovery – Participating in heavy drinking and experiencing a blackout does not mean that you have an AUD. Although, if this is a common occurrence, it may be time to seek addiction treatment. Substance abuse with alcohol can be a life-threatening disease and cause harmful effects on the body.
How long can a blackout last?
How Long Does a Power Outage Last? T he quick and mostly vague answer to this question is that most power outages last only a few minutes, but some can last for days or even up to a week. While this may seem like a broad time frame, numerous factors can affect how quickly you get your power back on.
- Depending on how well you know your utility company, you might be able to estimate the time of a power outage based on the following: The will almost certainly affect how long it takes for power restoration.
- Utility workers can fix a minor incident, such as a fallen power line, in around 2-3 hours.
- But when the cause of a blackout is severe weather or a natural disaster, you can expect to be out for several days and even months in some extreme cases.
If a power pole comes down, it could be at least a day before the utility company has it back up and running. A serious situation involving a whole power plant may leave you without electricity for around a week. Power from other plants is brought onto the grid to compensate for the lack of electricity if a plant explosion or incident causes a shutdown. After a storm or disaster, utility companies, like any industry, follow a series of steps to restore power for the most amount of people as soon as possible. After assessing the damage, repairing substations, and priority facilities such as hospitals, repair crews then start to restore power for customers.
More often than not, the closer you are to transmission lines, the faster you’ll get electricity. If your neighborhood has extensive damage, you may wait longer, especially if the problem only affects a few customers. In the case of natural disasters, where the damage is widespread, utility workers may also be spread thin.
Additionally, cities or urban areas likely have many more workers and appliances on hand to fix outages quickly. In the countryside or developing countries, lack of resources and skilled workers may delay repairs. Some line issues are digital and repaired quickly and remotely.
- Physical damage requires a manual repair, which takes much more time.
- Before fully restoring power, lineworkers need to perform tests that might cause power trips and overloading, making the repair phase even longer.
- When a grid overload causes a blackout, this requires more than just a fix.
- While these more significant grid issues are being addressed, utility companies arrange to avoid extended outages.
In this situation, customers still experience an outage, but for a shorter, fixed time of a few hours. Customers are usually notified that a rolling blackout will happen so they can prepare in advance. Whether you experience winter storms every year or live outside the urban sprawl, a power outage can strike at any time.
- You can keep your family safe and your home running smoothly with a rechargeable battery known as a,
- With large capacities and the ability to power high-wattage appliances, an can become your lifeline during an outage: Even when the gas and electricity are off, you can still prepare meals for your family using a microwave or hot plate.
Keep your home warm with heaters or electric blankets, and of course, keep your mobile phones and laptops charged. A can keep your refrigerator or chest freezer running for around a day so that you won’t lose groceries or frozen food. Although, they have limitations, especially during a natural disaster. Portable power stations, on the other hand, have fewer restrictions. There are no fumes or gas to store, so they’re safe to use inside to power your home during a storm. Since you can prep an EcoFlow portable power station in advance, they’re always ready when you need them.
- Recharge using a home AC outlet, solar panels, or in the case of DELTA Pro, from an EV charging station or Smart Generator.
- While you don’t have power, you can pull out to recharge your portable battery.
- No matter if it’s an hour outage or a week-long blackout, use your portable power station to keep all your home essentials running.
Compare our range of DELTA portable power stations to see which fits your needs best.
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|Coffee Machine (1000W)1.9 Hours|
|Air Fryer (1500W) 1.2 Hours|
img class=’aligncenter wp-image-189362 size-full’ src=’https://www.beerdelux.com/wp-content/uploads/2023/07/wecasypaezhicymimaetezhy.png’ alt=’What Is Blacking Out From Alcohol’ />
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: How Long Does a Power Outage Last?
Why do I blackout after 2 drinks?
What Is Blacking Out? – What does it mean when someone says that they were so drunk the night before that they “blacked out?” Blacking out is a period of alcohol -induced amnesia during which an intoxicated person actively engages in behaviors like walking or talking but doesn’t remember doing so.
Blackouts are most commonly caused by a rapid increase in blood alcohol concentration (BAC) levels, resulting in a temporary loss of memory. People normally experience a blackout when their BAC reaches around,14%, or,14 (point one four) which is almost twice the legal limit, In addition to blacking out, an individual can also suffer from milder alcohol -induced memory impairments, called “brownouts” or “grayouts.” It’s important to note that blacking out is different than passing out, as the person is fully conscious when blacked out.
In fact, anything a person can do when they are drunk, they can do while blacked out – they just simply won’t remember it the next day. However, during a blackout, a person will be able to remember events that happened before their BAC reached very high levels.
This allows people that are blacked out to carry on conversations and recall stories from earlier in the evening while they were intoxicated. Online Counseling for Alcohol Addiction Online therapy can help you with long term addiction support. Start your therapy journey with BetterHelp. Paid Advertising.
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Can I drink without getting drunk?
A happy hour with new co-workers (and your boss), Mother’s Day brunch, your nephew’s 3rd birthday party: These are just a few places where you might want to have a drink (or three) without slurring your words or telling the same story for the 20th time.
- Luckily for you, it’s totally possible to imbibe without getting drunk.
- To drink and not get drunk, you need to aim to keep your blood alcohol concentration (BAC) below,06 percent.
- A BAC of 0.06 percent is the sweet spot — also referred to as the green zone — because you’re able to enjoy the effects that make social drinking a good time without the negative effects of drinking too much.
It’s also under the legal limit in the United States, which is 0.08 percent in case you’re worried about driving (more on that later). Staying under,06 percent can make you feel relaxed and more sociable. Depending on your tolerance, you may also feel buzzed and your judgment may be slightly impaired, but you won’t be stumbling or slurring your words.
You’ll also be able to get better sleep and avoid a killer hangover the next morning so you can get on with your day. A BAC calculator can help you figure out how much you can drink to stay in the zone so you can set a drink limit. Seriously, you gotta eat. Drinking on an empty stomach is the last thing you want to do if you’re trying not to get drunk.
Food in the stomach helps slow alcohol absorption, which can keep your BAC down. Have a meal or at least a hearty snack before heading out to an event or night out, and continue to nosh while drinking. Some foods are better than others before drinking because, along with slowing alcohol absorption, they can also reduce your risk of booze-induced tummy issues, like heartburn and nausea, and help prevent a hangover.
The body typically takes an hour to process one standard drink. If you drink fast or chug your bevs, your body doesn’t have the time it needs to do this, resulting in a buildup of alcohol in your bloodstream and a higher BAC. Sipping your drinks slowly so that you’re not exceeding more than one drink per hour is the best way not to get drunk.
To help pace yourself, don’t order another drink or let someone refill your glass until it’s empty. Having ice in your glass will also slow you down (and water down the booze a tad). If you’re going to drink, alternating between alcoholic and nonalcoholic drinks is a great way to limit your intake and keep you from getting sloshed.
- Water is always a good way to go, but if you prefer something more festive, you’ve got options in the way of booze alternatives that’ll make alternating a pleasure.
- Mocktails are great if you’re more a tiny-umbrella-in-your-drink sort of person, but there’s more to booze alternatives than virgin coladas.
Nonalcoholic beer has come a long way. There are even nonalcoholic spirits and bitters worth subbing in if you like the taste of the harder stuff. If wine is more your jam, wine alcohol-removed options will let you enjoy your night through rosé-colored glasses instead of beer goggles,
- It sounds like hooey, but there’s some evidence that the shape of your glass may influence how much you drink.
- In one study, participants were 60 percent slower at drinking alcoholic drinks out of a straight glass than a curved one.
- Granted, the study was small, not performed IRL, and beer was the only alcoholic beverage included.
Still, it may be worth a try if you tend to knock back cold ones fast and would rather not. That said, glass shape may make a difference when it comes to mixed drinks, too, according to an older study from 2005. According to that study, people (professional bartenders included) unknowingly pour 20 to 30 percent more alcohol into short, wide glasses than tall, slender ones.
If you’re out for drinks and trying not to get drunk, it may be worth asking for your drink in a tall, narrow glass if possible. When mixing your own drinks, using a tall, slender glass or one with the alcohol level pre-marked may help keep you from accidentally underestimating your pour. We get the allure of doing shots, but they’re hands down the fastest way to end up capital-D drunk.
That’s because shots are up there in alcohol concentration, with most distilled spirits containing 40 percent alcohol. Plus, you knock ’em back super quick, which can raise your BAC real fast. Seriously, if you’re trying not to get drunk, say no to shots.
- Even if you keep your alcohol limit below the legal limit, that doesn’t mean you’re fit to drive.
- You can still be impaired even without feeling drunk.
- Yes, even if you keep your BAC below the,06 percent sweet spot we covered earlier.
- Judgment impairment actually begins well below that, at a BAC of around,02 percent — which is also well below the legal limit for driving.
The impact alcohol has on a person, from how fast it kicks in and wears off to how severe the effects are, can vary significantly due to factors including:
sex assigned at birthbody size and compositionageoverall healthgeneticswhether you’ve eatenhow hydrated you arewhether you’re taking certain medications or mixing alcohol with other substances
Even if you have no intention of getting drunk, making arrangements for a ride home is a good idea if you’re going to be drinking. Another option is to arrange a place to stay until you’re sober and it’s safe to drive again. You can get your drink on and not get drunk by keeping tabs on how much alcohol is in your drinks and pacing yourself accordingly.
Talk with your primary care doctor.Call SAMHSA ‘s National Helpline at 800-662-4357 for treatment referral and info.Use the NIAAA Alcohol Treatment Navigator to find support.
How do you pass out drunk?
When someone drinks too much alcohol or too quickly, it can overwhelm or suppress the healthy performance of these systems in the body. This can lead to the person passing out or having alcohol poisoning. A person can die from alcohol poisoning if their respiratory system (breathing) shuts down.
Is blacking out an emergency?
Fainting occurs when the brain doesn’t receive enough blood for a brief time. This causes loss of consciousness. Consciousness is usually regained quickly. Fainting might have no medical significance. Or the cause can be a serious disorder, occasionally involving the heart.
Can anxiety cause blackouts?
Feel like passing out, including feeling faint or that you might suddenly blackout is a common symptom of anxiety disorder, including generalized anxiety disorder, social anxiety disorder, panic disorder, and others. This article explains the relationship between anxiety and the feel like passing out anxiety symptom.
What is the difference between black out and pass out?
Answer: Blacking out is a loss of memory – not being able to remember what happened because your brain has lost the ability to form new memories due to intoxication. Passing out is losing consciousness and not being able to be awakened.
What happens when you drink too much alcohol at once?
What Is an Alcohol Overdose? – An alcohol overdose occurs when there is so much alcohol in the bloodstream that areas of the brain controlling basic life-support functions—such as breathing, heart rate, and temperature control—begin to shut down. Symptoms of alcohol overdose include mental confusion, difficulty remaining conscious, vomiting, seizures, trouble breathing, slow heart rate, clammy skin, dulled responses (such as no gag reflex, which prevents choking), and extremely low body temperature.
- Alcohol overdose can lead to permanent brain damage or death.
- What tips the balance from drinking that produces impairment to drinking that puts one’s life in jeopardy varies among individuals.
- Age, sensitivity to alcohol (tolerance), gender, speed of drinking, medications you are taking, and amount of food eaten can all be factors.
Alcohol use and taking opioids or sedative hypnotics, such as sleep and anti-anxiety medications, can increase your risk of an overdose. Examples of these medications include sleep aids, such as zolpidem and eszopiclone, and benzodiazepines, such as diazepam and alprazolam.
Even drinking alcohol while taking over-the-counter antihistamines can be dangerous. Using alcohol with opioid pain relievers, such as oxycodone and morphine, or illicit opioids, such as heroin, is also a very dangerous combination. Like alcohol, these drugs suppress areas in the brain that control vital functions such as breathing.
Ingesting alcohol and other drugs together intensifies their individual effects and could produce an overdose with even moderate amounts of alcohol. Image
Why do I forget when I drink?
Aaron M. White, Ph.D. – Aaron M. White, Ph.D., is an assistant research professor in the Department of Psychiatry, Duke University Medical Center, Durham, North Carolina. This work was supported by the National Institute on Alcohol Abuse and Alcoholism grant AA–12478 and the Institute for Medical Research at the VA Medical Center in Durham, North Carolina.
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 auotbiographical memories. Key words: alcoholic blackout; memory interference; AOD (alcohol and other drug) intoxication; AODE (alcohol and other drug effects); AODR (alcohol and other drug related) mental disorder; long–term memory; short–term memory; state–dependent memory; BAC level; social AOD use; drug interaction; disease 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 diversity of symptoms that may ensue from the action 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 one or two drinks. As the dose increases, so does the magnitude of the memory impairments.
- Under certain circumstances, alcohol can disrupt or completely block the ability to form memories for events that transpire while a person is intoxicated, a type of impairment known as a blackout.
- This article reviews what is currently known regarding the specific features of acute alcohol–induced memory dysfunction, particularly alcohol–induced blackouts, and the pharmacological mechanisms underlying them.
EFFECTS OF ALCOHOL ON MEMORY To evaluate the effects of alcohol, or any other drug, on memory, one must first identify a model of memory formation and storage to use as a reference. One classic, often–cited model, initially proposed by Atkinson and Shiffrin (1968), posits that memory formation and storage take place in several stages, proceeding from sensory memory (which lasts up to a few seconds) to short–term memory (which lasts from seconds to minutes depending upon whether the information is rehearsed) to long–term storage.
- This model often is referred to as the modal model of memory, as it captures key elements of several other major models.
- Indeed, elements of this model still can be seen in virtually all models of memory formation.
- In the modal model of memory, when one attends to sensory information, it is transferred from a sensory memory store to short–term memory.
The likelihood that information will be transferred from short–term to long–term storage, or be encoded into long–term memory, was once thought to depend primarily on how long the person keeps the information active in short–term memory via rehearsal.
Although rehearsal clearly influences the transfer of information into long–term storage, it is important to note that other factors, such as the depth of processing (i.e., the level of true understanding and manipulation of the information), attention, motivation, and arousal also play important roles (Craik and Lockhart 1972; Otten et al.2001; Eichenbaum 2002).1 ( 1 It 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 memory using a three–stage process of memory formation akin to the modal model. The interpretation of the effects of alcohol on memory likely would vary somewhat depending on the memory model one uses.) Variability in the use of terms, particularly in operational definitions of short–term memory, makes it difficult to formulate a simple synopsis of the literature on alcohol–induced memory impairments.
As Mello (1973) stated three decades ago with regard to the memory literature in general, “The inconsistent use of descriptive terms has been a recurrent source of confusion in the ‘short–term’ memory literature and ‘short–term’ memory has been variously defined as 5 seconds, 5 minutes, and 30 minutes” (p.333).
In spite of this inconsistency, several conclusions can be drawn from research on alcohol–induced memory impairments. One conclusion is that the impact of alcohol on the formation of new long–term “explicit” memories—that is, memories of facts (e.g., names and phone numbers) and events—is far greater than the drug’s impact on the ability to recall previously established memories or to hold new information in short–term memory (Lister et al.1991).
(See figure 1 for a diagram depicting the stages of memory and where alcohol interferes with memory.) Intoxicated subjects are typically able to repeat new information immediately after its presentation and often can keep it active in short–term storage for up to a few minutes if they are not distracted (for an early 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 contrast, alcohol impairs the ability to store information 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 example, the letter “B” paired with the month “January”—they were impaired when asked to recall the items after delays of a minute or more. However, subjects could recall paired associates that they had learned before becoming intoxicated.
More recently, Acheson and colleagues (1998) observed that intoxicated subjects could recall items on word lists immediately after the lists were presented but were impaired when asked to recall the items 20 minutes later.
|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.|
Ryback (1971) characterized the impact of alcohol on memory formation as a dose–related continuum, with minor impairments at one end and large impairments at the other, all impairments representing the same fundamental deficit in the ability to transfer new information from short–term to long–term storage.
When doses of alcohol are small to moderate (producing blood alcohol concentrations below 0.15 percent), memory impairments tend to be small to moderate as well. At these levels, alcohol produces what Ryback (1971) referred to as 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 word lists or learning to recognize new faces (Westrick et al.1988; Mintzer and Griffiths 2002). As the dose increases, the resulting memory impairments can become much more profound, sometimes culminating in blackouts—periods for which a person is unable to remember critical elements of events, or even entire events, that occurred while he or she was intoxicated.
Alcohol–Induced Blackouts Blackouts represent episodes of amnesia, during which subjects are capable of participating even in salient, emotionally charged events—as well as more mundane events—that they later cannot remember (Goodwin 1995). Like milder alcohol–induced memory impairments, these periods of amnesia are primarily “anterograde,” meaning that alcohol impairs the ability to form new memories while the person is intoxicated, but does not typically erase memories formed before intoxication.
Formal research into the nature of alcohol–induced blackouts began in the 1940s with the work of E.M. Jellinek (1946). Jellinek’s initial characterization of blackouts was based on data collected from a survey of Alcoholics Anonymous 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 most influential studies in the literature on blackouts (Goodwin et al.1969 a,b ).
- Based on interviews with 100 hospitalized alcoholics, 64 of whom had a history of blackouts, the authors posited the existence of two qualitatively different types of blackouts: en bloc and fragmentary blackouts.
People experiencing en bloc blackouts are unable to recall any details whatsoever 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 formation, it is as if the process of transferring information from short–term to long–term storage has been completely blocked.
- En bloc memory impairments tend to have a distinct onset.
- It is usually less clear when these blackouts end because people typically fall asleep before they are over.
- Interestingly, people appear able to keep information active in short–term memory for at least a few seconds.
- As a result, they can often carry on conversations, drive automobiles, and engage in other complicated behaviors.
Information pertaining to these events is simply not 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 not remember what they said or did 5 minutes earlier.
- Their immediate and remote memory 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 2 minutes while the sessions were taking place.
Unlike en bloc blackouts, fragmentary blackouts involve partial blocking of memory formation for events that occurred while the person was intoxicated. Goodwin and colleagues (1969 a ) reported that subjects experiencing fragmentary blackouts often become aware that they are missing pieces of events only after being reminded that the events occurred.
- Interestingly, these reminders trigger at least some recall of the initially missing information.
- Research suggests that fragmentary blackouts are far more common than those of the en bloc variety (White et al.2004; Hartzler and Fromme 2003 b ; Goodwin et al.1969 b ).
- Blackouts: State–Dependent Memory Formation? Early anecdotal evidence suggested that blackouts might actually reflect state–dependent information storage—that is, people might be able to remember events that occurred while they were intoxicated if they returned to that state (e.g., Goodwin et al.1969 a ).
State–dependent memory can be viewed as a special case of a broader category known as context–dependent memory (e.g., White et al.2002 a ), in which cues that are associated with an event when a memory is formed tend to help trigger recall for that event at a later time.
- For instance, in a classic study by Godden and Baddeley (1975) divers who learned word lists either on land or under water remembered more words when tested in the same context in which learning took place (i.e., land–land or water–water).
- Likewise, returning to the same emotional or physiological state that was present when a memory was formed often can facilitate recall of that memory.
It is not uncommon to hear stories of drinkers who stash alcohol or money while intoxicated and can locate the hiding places only after becoming intoxicated again (Goodwin 1995). Regardless of how compelling such stories can be, clear evidence of state–dependent learning under the influence of alcohol is lacking.
- In one recent study, Weissenborn and Duka (2000) examined whether subjects who learned word lists while intoxicated could recall more items if they were intoxicated again during the testing session.
- No such state–dependency was observed.
- Similarly, Lisman (1974) tried unsuccessfully to help 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 often precedes blackouts, but several other factors also appear to play important roles in causing such episodes of memory loss. As Goodwin and colleagues (1969 a ) stated with regard to subjects in one of their studies, “Although blackouts almost always were associated with heavy drinking, this alone seemed insufficient to produce one.
- On many other occasions, subjects said they had drunk as much or more without memory loss” (p.195).
- Among the factors that preceded blackouts were gulping drinks and drinking on an empty stomach, each of which leads to a rapid rise in BAC.
- Subsequent research provided additional evidence suggesting a link between blackouts and rapidly rising BACs.
Goodwin and colleagues (1970) examined the impact of acute alcohol exposure on memory formation in a laboratory setting. The author recruited 10 male subjects for the project, all but one through the unemployment office in St. Louis, Missouri. Most subjects met diagnostic criteria for alcoholism and half had a history of frequent blackouts.
The men were asked to consume roughly 16 to 18 ounces of 86–proof bourbon in approximately 4 hours. Beginning 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 recall details regarding these stimuli 2 minutes, 30 minutes, and 24 hours after the stimuli were shown.
Half of the subjects reported no recall for the stimuli or their presentation 30 minutes and 24 hours after the events, though most seemed to recall the stimuli 2 minutes after presentation. Lack of recall for the events 24 hours later, while sober, represents clear experimental evidence 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 short–term to long–term storage. For all but one subject in the blackout group, memory impairments began during the first few hours of drinking, when BAC levels were still rising.
The average peak BAC in this group, which was roughly 0.28 percent, occurred approximately 2.5 hours after the onset of drinking. In a similar study, Ryback (1970) examined the impact of alcohol on memory in seven hospitalized alcoholics given access to alcohol over the course of several days.
- All subjects were White males between the ages of 31 and 44.
- Blackouts occurred in five of the seven subjects, as evidenced by an inability to recall salient events that occurred while drinking the day before (e.g., one subject could not recall preparing to hit another over the head with a chair).
- Estimates of BAC levels during blackout periods suggested that they often began at levels around 0.20 percent and as low as 0.14 percent.
The duration of blackouts ranged from 9 hours to 3 days. Based on his observations, Ryback concluded that a key predictor of blackouts was the rate at which subjects consumed their drinks. He stated, “It is important to note that all the blackout periods occurred after a rapid rise in blood alcohol level” (p.622).
- The two subjects who did not black out, despite becoming extremely intoxicated, experienced slow increases in blood alcohol levels.
- Blackouts Among Social Drinkers Most of the research conducted on blackouts during the past 50 years has involved surveys, interviews, and direct observation of middle–aged, primarily male alcoholics, many of whom were hospitalized.
Researchers have largely ignored the occurrence of blackouts among young social drinkers, so the idea that blackouts are an unlikely consequence of heavy drinking in nonalcoholics has remained deeply entrenched in both the scientific and popular cultures.
- Yet there is clear evidence that blackouts do occur among social drinkers.
- Night 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–year medical students he interviewed acknowledged having had at least one 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) found that 35 percent of all males surveyed had had at least one blackout in the year before the survey.
As might be expected given the excessive drinking habits of many college students (Wechsler et al.2002), this population commonly experiences blackouts. White and colleagues (2002 c ) recently surveyed 772 undergraduates regarding their experiences with blackouts. Respondents who answered yes to the question “Have you ever awoken after a night of drinking not able to remember things that you did or places that you went?” were considered to have experienced blackouts.
Fifty–one percent of the students who had ever consumed alcohol reported blacking out at some point in their lives, and 40 percent reported experiencing a blackout in the year before the survey. Of those who had consumed alcohol during the 2 weeks before the survey, 9.4 percent reported blacking out during this period.
Students in the study reported that they later 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 automobile, and spending money. During the 2 weeks preceding the survey, an equal percentage 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 black out likely arises, in part, from well–known gender differences in physiological factors that affect alcohol distribution and metabolism, such as body weight, proportion of body fat, and levels of key enzymes.
- There also is some evidence that females are more susceptible than males to milder forms of alcohol–induced memory 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 blackout, to gather more information about the factors related to blackouts.
As in the previous study, students reported engaging in a range of risky behaviors during blackouts, including sexual activity with both acquaintances and strangers, vandalism, getting into arguments and fights, and others. During the night of their most recent blackout, most students drank either liquor alone or in combination with beer.
- Only 1 student out of 50 reported that the most recent blackout occurred after drinking beer alone.
- On average, students estimated that they consumed roughly 11.5 drinks before the onset of the blackout.
- Males reported drinking significantly more than females, but they did so over a significantly longer period of time.
As a result, estimated peak BACs during the night of the last blackout were similar for males (0.30 percent) and females (0.35 percent). As Goodwin observed in his work with alcoholics (1969 b ), 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 blackout was of waking up in the morning, often in an unfamiliar location.
- Many students, more females (59 percent) than males (25 percent), were frightened by their last blackout and changed their drinking habits as a result.
Use of Other Drugs During Blackouts Alcohol interacts with several other drugs, many of which are capable of producing amnesia on their own. For instance, diazepam (Valium ® ) and flunitrazepam (Rohypnol) are benzodiazepine sedatives that can produce severe memory impairments at high 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 increase 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 alone (Ciccocioppo et al.2002).
Given that many college 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 alone. Indeed, based on interviews with 136 heavy–drinking young adults (mean age 22), Hartzler and Fromme (2003 b ) concluded that en bloc blackouts often arise from the combined use of alcohol and other drugs.
- White and colleagues (2004) observed that, among 50 undergraduate students with a history of blackouts, only 3 students reported using other drugs during the night of their most recent blackout, and marijuana was the drug in each case.
- Are Some People More Likely Than Others to Experience Blackouts? In classic studies of hospitalized alcoholics by Goodwin and colleagues (1969 a,b ), 36 out of the 100 patients interviewed indicated that they had never experienced a blackout.
In some ways, the patients who did not experience blackouts are as interesting as the patients who did. What was it about 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 but simply were unaware of them, there may have been something fundamentally different about these patients that diminished their likelihood of experiencing memory impairments while drinking.
In support of this possibility, a recent study by Hartzler and Fromme (2003 a ) suggests that people with a history of blackouts are more vulnerable to the effects of alcohol 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 year.
While sober, members of the two groups performed comparably in memory tasks. However, when they were mildly intoxicated (0.08 percent BAC) those with a history of fragmentary blackouts performed worse than those without such a history. There are two possible interpretations for these data, both of which support the hypothesis that some people are more susceptible to blackouts than others.
One plausible interpretation is that subjects in the fragmentary blackout group always have been more vulnerable to alcohol–induced memory impairments, which is why they performed poorly during testing under alcohol, and why they are members of the blackout group in the first place. A second interpretation is that subjects in the blackout group performed poorly during testing as a result of drinking enough in the past to experience alcohol–induced memory impairments.
In other words, perhaps their prior exposure to alcohol damaged the brain in a way that predisposed them to experiencing future memory impairments. This latter possibility is made more likely by recent evidence that students who engage in repeated episodes of heavy, or binge, drinking are more likely than other students to exhibit memory impairments when they are intoxicated (Weissenborn and Duka 2000).
Similar results have been observed in animal studies (White et al.2000 a ). The argument for an inherent vulnerability to alcohol–induced memory impairments, including blackouts, is strengthened by two recent studies. In an impressive longitudinal study, Baer and colleagues (2003) examined the drinking habits of pregnant women in 1974 and 1975, and then studied alcohol use and related problems in their offspring at seven different time points during the following 21 years.
These authors observed that prenatal alcohol exposure was associated with increased rates of experiencing alcohol–related consequences, including blackouts, even after controlling for the offsprings’ general drinking habits. In addition, a recent report by Nelson and colleagues (2004) suggests that there might actually be a genetic contribution to the susceptibility to blackouts, indicating that some people simply are built in a way that makes them more vulnerable to alcohol–induced amnesia.
As discussed in the section below on the potential brain mechanisms underlying alcohol–induced amnesia, it is easy to imagine that the impact of alcohol on brain circuitry could vary from person to person, rendering some people more sensitive than others to the memory–impairing effects of the drug. HOW DOES ALCOHOL IMPAIR MEMORY? During the first half of the 20th century, two theoretical hurdles hampered progress toward an understanding of the mechanisms underlying the effects of alcohol on memory.
More recent research has cleared away 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.M., it became clear that different brain regions are involved in the formation, storage, and retrieval of different types of memory.
- In 1953, large portions of H.M.’s 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 by the surgery, it soon became clear that H.M.
suffered from a dramatic syndrome of memory impairments. He still was able to learn basic motor skills, keep information active in short–term memory 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 pattern of H.M.’s impairments also forced a re–examination of models of long–term memory 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 within the year preceding his surgery.
- This strongly suggests that the transfer of information into long–term storage actually takes place over several years, with the hippocampus being necessary for its retrieval for the first year or so.
Subsequent research with other patients confirmed that the hippocampus, an irregularly shaped structure deep in the forebrain, is critically involved in the formation of memories for events (see 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 as 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 small region of the hippocampus called hippocampal 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 assist the hippocampus in communicating with other areas of the brain. 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 brain structures.
(Neocortex literally means “new bark” or “new covering.” When one looks at a picture of the human brain, most of what is visible is neocortex.) The hippocampus somehow ties information from other brain regions together to form new autobiographical memories, and CA1 pyramidal cells send the results of this processing back out to the neocortex.
As is clear from patient R.B., removing CA1 pyramidal cells from the circuitry prevents the hippocampal memory system from doing its job.
|Figure 2 The human brain, showing the location of the hippocampus, the frontal lobes, and the medial septum.|
The second barrier to understanding the mechanisms underlying alcohol’s effects on memory was an incomplete understanding of how alcohol affects brain function at a cellular level. Until recently, alcohol was assumed to affect the brain in a general way, simply shutting down the activity of all cells with which it came in contact.
The pervasiveness of this assumption is reflected in numerous writings during the early 20th century. For instance, Fleming (1935) wrote, “The prophetic generalization of Schmiedeberg in 1833 that the pharmacological action of alcohol on the cerebrum is purely depressant has been found, most pharmacologists will agree, to characterize its action in 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 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.g., Chin and Goldstein 1977).
This view persisted into the late 1980s, at which time the consensus began to shift as evidence mounted that alcohol has selective effects on the brain’s nerve–cell communication (i.e., neurotransmitter) systems, altering activity in some types of receptors but not others (e.g., Criswell et al.1993).
Substantial evidence now indicates that alcohol selectively alters the activity of specific complexes of proteins embedded in the membranes of cells (i.e., receptors) that bind neurotransmitters such as gamma–aminobutyric acid (GABA), glutamate, serotonin, acetylcholine, and glycine (for a review, see Little 1999).
In some cases, only a few amino acids appear to distinguish receptors that are sensitive to alcohol from those that are not (Peoples and Stewart 2000). It remains unclear exactly how alcohol interacts with receptors to alter their activity. Alcohol, Memory, and the Hippocampus More than 30 years ago, both Ryback (1970) and Goodwin and colleagues (1969 a ) 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 damage. Specifically, both acute alcohol exposure and hippocampal damage impair the ability to form new long–term, explicit memories but do not affect short–term memory storage or, in general, the recall of information from long–term storage.
Research conducted in the past few decades using animal models supports the hypothesis that alcohol impairs memory formation, at least in part, by disrupting activity in the hippocampus (for a review, see White et al.2000 b ). Such research has included behavioral observation; examination of slices of and brain tissue, neurons in cell culture, and brain activity in anesthetized or freely behaving animals; and a variety of pharmacological techniques.
As mentioned above, damage limited to the CA1 region of the hippocampus dramatically disrupts the ability to form 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 result in one cell communicating with other cells (i.e., action 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 action potentials primarily when the rat is at the far end of the north arm, while another might generate action potentials primarily when the rat is in the middle of the south arm, and so on.
Collectively, the cells that are active in that particular environment create a spatial, or contextual map that serves as a framework for event memories created in that environment. Because of the location–specific firing of these cells, they often are referred to as “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 important to the formation of memories for facts and events, and the clear behavioral correlates of their activity in rodents, it is possible to assess the impact of alcohol on hippocampal output in an intact, fully functional brain by studying these cells.
In recent work with awake, freely behaving rats, White and Best (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.e., microelectrodes) implanted in their brains.
- Figure 3 displays the activity of an individual CA1 pyramidal cell.
- The activity—which corresponds to the middle portion of the lower left arm of the maze—is shown before alcohol administration (A), 45 to 60 minutes after alcohol administration (B), and 7 hours after alcohol administration (C).
- The dose of alcohol used in the testing session was 1.5 grams per kilogram of body weight—enough to produce a peak BAC of about 0.16 percent.
(A corresponding BAC in humans would be twice the legal driving limit in most States.) As the figure illustrates, the cell’s activity was essentially shut off by alcohol. Neural activity returned to near–normal levels within about 7 hours of alcohol administration.
|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.|
White and Best administered several doses of alcohol in this study, ranging from 0.5 g/kg to 1.5 g/kg. (Only one of the experiments is represented in figure 3.) They found that the dose affected the degree of pyramidal cell suppression. Although 0.5 g/kg did not produce a significant change in the firing of hippocampal pyramidal cells, 1.0 and 1.5 g/kg produced significant suppression of firing during a 1–hour testing session following alcohol administration.
The dose–dependent suppression of CA1 pyramidal cells is consistent with the dose–dependent effects of alcohol on episodic memory formation. Alcohol and Hippocampal Long–Term Potentiation In addition to suppressing the output from pyramidal cells, alcohol has several other effects on hippocampal function.
For instance, 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). Because researchers have theorized that something like LTP occurs naturally in the brain during learning (for a review, see Martin and Morris 2002), many investigators have used LTP as a model for studying the neurobiology underlying the effects of drugs, including alcohol, on memory.
In a typical LTP experiment, two electrodes (A and B) are lowered into a slice of hippocampal tissue kept alive by bathing it in oxygenated artificial cerebral spinal fluid (ACSF). A small amount of current is passed through electrode A, causing the neurons in this area to send signals to cells located near electrode B.
Electrode B then is used to record how the cells in the area respond to the incoming signals. This response is the baseline response. Next, a specific pattern of stimulation intended to model the pattern of activity that might occur during an actual learning event 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, as 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 often lasts for an extended period 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 impairment begins at concentrations equivalent to those produced by 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 later at position B will not be larger than it was at baseline (that is, it will not be potentiated).
- And, just as alcohol tends not to impair recall of memories established before alcohol exposure, alcohol does not disrupt the expression of LTP established before alcohol exposure.
One of the key requirements for the establishment of LTP in the hippocampus is that a type of signal receptor known as the NMDA 2 receptor becomes activated. ( 2 N –methyl–D–aspartate is a receptor for the neurotransmitter glutamate.) Activation of the NMDA receptor allows calcium to enter the cell, which sets off a chain of events leading to long–lasting changes in the cell’s structure or function, 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 primary mechanism underlying the effects of alcohol on LTP, though other transmitter systems probably are also involved (Schummers and Browning 2001).
Indirect Effects of Alcohol on Hippocampal Function Like other brain regions, the hippocampus does not operate in isolation. Information processing in the hippocampus depends on coordinated input from a variety of other structures, which gives alcohol and other drugs additional opportunities to disrupt hippocampal functioning.
One brain region that is central to hippocampal functioning is a small 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 activity, 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 thought to act as a gatekeeper, increasing or decreasing the likelihood that information entering the hippocampus from cortical structures will be processed (Orr et al.2001).
(For more information on the role of electrophysiology in diagnosing alcohol problems, see the article in this issue by Porjesz and Begleiter.) Information entering 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 ability to perform tasks that depend on the hippocampus (Givens et al.2000). Alcohol disrupts the theta rhythm in large part 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 activity in the medial septum is likely to play an important role in the effects of alcohol on memory. 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 Memory Impairments The hippocampus is not the only structure involved in memory 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 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 all have 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 one–time (i.e., acute) 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 (Kahkonen et al.2003).
Although the exact meaning of these changes remains unclear, the evidence suggests that acute intoxication alters the normal functioning of the frontal lobes. 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 involved in alcohol–induced memory impairment.
- SUMMARY AND CONCLUSIONS As detailed in this brief review, alcohol can have a dramatic impact on memory.
- Alcohol primarily disrupts the ability to form new long–term memories; it causes less disruption of recall of previously established long–term memories or of the ability to keep new information active in short–term memory for a few seconds or more.
At low doses, the impairments produced by alcohol are often subtle, though they are detectable in controlled conditions. As the amount of alcohol consumed increases, so does the magnitude of the memory impairments. Large quantities of alcohol, particularly if consumed rapidly, can produce a blackout, an interval of time for which the intoxicated person cannot recall key details of events, or even entire events.
- En bloc blackouts are stretches of time for which the person has no memory whatsoever.
- Fragmentary blackouts are episodes for which the drinker’s memory is spotty, with “islands” of memory providing some insight into what transpired, and for which more recall usually is possible if the drinker is cued by others.
Blackouts are much more common among social drinkers than previously assumed and should be viewed as a potential consequence 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 memory 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 impact of alcohol on the frontal lobes remains poorly understood, but probably plays an important 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 impact of drugs like alcohol on brain 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 by factors such as attention and motivation (e.g., Kensinger et al.2003). With the aid of neuroimaging techniques, researchers may be able to examine the impact of alcohol on brain activity related to these factors, and then determine how alcohol contributes to memory impairments.
Despite advances in human neuroimaging techniques, animal models remain absolutely essential in the study of mechanisms underlying alcohol–induced memory impairments. Hopefully, future work will reveal more 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 allow for recordings from hundreds of individual cells in several brain regions simultaneously (Kralik et al.2001), could provide much–needed information regarding the impact of alcohol on the interactions between disparate brain regions involved in the encoding, storage, and retrieval of information.
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Why do people get drunk?
In the brain, alcohol acts as a depressant, slowing brain responses. This is what causes the feeling of being ‘drunk.’ Using safer drinking practices can help your body process the alcohol you drink and avoid severe intoxication.