Charles F. Zorumski, head of the department of psychiatry at the Washington University School of Medicine in St. Louis, answers:
It is indeed possible for a person to get intoxicated and not remember what she or he did. This state is called a “blackout” or, more precisely, a “memory blackout.” During a blackout a person is intoxicated but awake and interacting with the environment in seemingly meaningful ways, such as holding a conversation or driving a car. After the period of intoxication, usually the next day, the person has no or, at best, vague recall for events that occurred while inebriated. At times, being in this state can have disastrous consequences, such as waking up in an unknown or unsafe place, losing personal possessions or participating in risky behaviors.
On the neural level, a blackout is a period of anterograde amnesia. That is, a person's ability to form new memories becomes impaired. Although a person does not lose previously learned information, he or she may also find it more difficult to recall certain facts while intoxicated. Yet once a person sobers up, his or her memory and ability to learn new information are not permanently affected.
How alcohol, or ethanol, produces a memory blackout is not completely understood. It is clear, however, that alcohol can impair a process in brain cells called long-term potentiation (LTP), a cellular mechanism thought to underlie memory formation, particularly in the hippocampus.
The amount of alcohol required to impair LTP and learning, and potentially cause a blackout, can vary. Important factors include the type and amount of alcohol consumed—high-potency drinks are worse—and the rate at which alcohol is consumed, with rapid consumption being more problematic. These factors affect how quickly alcohol levels rise in the brain and impair memory formation.
In our studies in rodents, blocking LTP in the hippocampus requires dangerously high concentrations of alcohol, about three times the level necessary to get a person drunk. It is important to note, however, that drugs other than alcohol can affect LTP. And when combined with alcohol, these drugs can cause blackouts at lower concentrations of alcohol. Common sedatives such as the benzodiazepines Xanax and Valium and drugs that act similarly on the brain, including the popular sleeping aid Ambien, can even induce a blackout on their own.
Given the dangers associated with blackouts, the best strategy to avoid having one is to abstain from heavy consumption and from combining alcohol with other neuroactive drugs.
It is indeed possible for a person to get intoxicated and not remember what she or he did. This state is called a “blackout” or, more precisely, a “memory blackout.” During a blackout a person is intoxicated but awake and interacting with the environment in seemingly meaningful ways, such as holding a conversation or driving a car. After the period of intoxication, usually the next day, the person has no or, at best, vague recall for events that occurred while inebriated. At times, being in this state can have disastrous consequences, such as waking up in an unknown or unsafe place, losing personal possessions or participating in risky behaviors.
On the neural level, a blackout is a period of anterograde amnesia. That is, a person's ability to form new memories becomes impaired. Although a person does not lose previously learned information, he or she may also find it more difficult to recall certain facts while intoxicated. Yet once a person sobers up, his or her memory and ability to learn new information are not permanently affected.
How alcohol, or ethanol, produces a memory blackout is not completely understood. It is clear, however, that alcohol can impair a process in brain cells called long-term potentiation (LTP), a cellular mechanism thought to underlie memory formation, particularly in the hippocampus.
The amount of alcohol required to impair LTP and learning, and potentially cause a blackout, can vary. Important factors include the type and amount of alcohol consumed—high-potency drinks are worse—and the rate at which alcohol is consumed, with rapid consumption being more problematic. These factors affect how quickly alcohol levels rise in the brain and impair memory formation.
In our studies in rodents, blocking LTP in the hippocampus requires dangerously high concentrations of alcohol, about three times the level necessary to get a person drunk. It is important to note, however, that drugs other than alcohol can affect LTP. And when combined with alcohol, these drugs can cause blackouts at lower concentrations of alcohol. Common sedatives such as the benzodiazepines Xanax and Valium and drugs that act similarly on the brain, including the popular sleeping aid Ambien, can even induce a blackout on their own.
Given the dangers associated with blackouts, the best strategy to avoid having one is to abstain from heavy consumption and from combining alcohol with other neuroactive drugs.
Eleine Ng, Singapore
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