Alcohol Effects on Brain : Adolescents, Part 2

by National Institute of Health

(Page 5 of 6)

Mechanisms That May Contribute to Reduced Motor-Impairing
and Sedative Effects in Adolescents

Researchers have not yet identified the mechanisms that account for the fact that adolescents are less susceptible to alcohol-related motor impairment and sedation than older individuals. It is likely, however, that the neurotransmitter GABA and its receptors play a role in both of these effects. As mentioned earlier, GABA is an inhibitory neurotransmitter, and the activity of GABA and its receptors is enhanced by alcohol. As a result, the GABA system has been implicated in both alcohol's sedative and its motor-impairing effects. Studies using rats have found that the levels of GABA receptors in various brain structures, including the cerebellum, increase markedly throughout adolescence and reach their final levels during early adulthood. Thus, it appears possible that adolescent rats are less sensitive to alcohol-induced motor impairment and sedation because, compared with older animals, they have fewer GABA receptors on which alcohol can act. Another possibility is that the function of GABA receptors is altered across adolescent development in a way that results in increased sensitivity to alcohol as the animal gets older.

The combination of reduced sensitivity to alcohol's motor-impairing and sedative effects on the one hand and increased sensitivity to alcohol's memory-impairing effects on the other hand could be particularly harmful to adolescents. For most people, the maximum amount of alcohol they can consume is determined by alcohol's motor-impairing and sedative effects - that is, if they do not stop drinking voluntarily, drinkers at some point become so incapacitated that they cannot continue to drink even if they want to. If, like adolescent animals, human adolescents also are less sensitive to these alcohol effects, it appears plausible that they might continue to drink longer than adults, achieving higher blood alcohol concentrations in the process. As a result, the adolescents could become even more vulnerable to the effects of alcohol on memory and other functions to which they are more susceptible than adults even at lower blood alcohol levels.

Susceptibility to Seizures During Withdrawal

Like all neurotransmitters, GABA has numerous functions and effects in regulating brain activity. For example, in addition to playing a role in motor impairment and sedation, GABA also is involved in the development of seizures during alcohol withdrawal. Long-term drinking causes the body to adjust to the continued presence of alcohol so that it eventually functions normally only in the presence of the drug. At that point, cessation of drinking can lead to an array of adverse symptoms, collectively called withdrawal, which include symptoms mediated by GABA.

Because alcohol stimulates the activity of GABA receptors, long-term drinking causes the brain to produce fewer of these receptors. If alcohol then is withheld, GABA activity suddenly drops off because fewer GABA receptors are available and alcohol no longer activates the ones that remain. This insufficient GABA activity has been linked to the development of seizures during withdrawal. If adolescents are less sensitive than adults to alcohol's effects on GABA and its receptors, adolescents also should be less prone to seizures during withdrawal from alcohol.

This hypothesis has been investigated in rats. For these experiments, Acheson and colleagues administered alcohol to adolescent and adult rats for 5 days, then injected the animals with a chemical that induces seizures and rated the severity and duration of the seizures. The study found that although adolescent and adult animals experienced seizures of various severities at a similar rate, the more severe seizures lasted significantly longer in the adult animals than in the adolescent animals. Thus, this study supports the hypothesis that adolescent animals are less sensitive than adults to alcohol's effects on the GABA system.

Alcohol Exposure during Adolescence
Affects Brain Function during Adulthood

When investigating alcohol's effects on the adolescent brain, it is important not only to focus on the immediate effects (e.g., memory impairment, motor impairment, or sedation) but also to explore the consequences of alcohol use on the adolescent's future development. Because the brain undergoes such extensive changes and remodeling during adolescence, it is reasonable to assume that disruption of these processes by alcohol could lead to long-term alterations that influence adult behavior and responses to alcohol.

The preceding sections have described how acute alcohol exposure affects the body differently during adolescence than during adulthood, with adolescents being more sensitive to some effects of alcohol and less sensitive to others. In addition, adolescents may respond differently to repeated heavy alcohol exposure, a drinking pattern also known as chronic intermittent exposure or binge drinking, which is particularly common among adolescents. Binge drinking is characterized by repeated episodes of heavy drinking followed by withdrawal. Several lines of evidence suggest that these repeated withdrawal episodes contribute to many of the effects of chronic alcohol exposure on the brain.

In one study of the long-term consequences of binge drinking during adolescence, White and colleagues studied animals that were repeatedly exposed to high levels of alcohol during adolescence. The alcohol-exposed and control animals were evaluated as adults with respect to alcohol's effects on motor activity, using the tilted plane test. As mentioned earlier, adult rats normally are more sensitive than adolescents to alcohol-induced motor impairment (i.e., the rats' sensitivity to motor impairment increases between adolescence and adulthood). This study found, however, that rats repeatedly exposed to alcohol during adolescence did not show this increase in sensitivity to alcohol's effects; these animals performed as well on the tilted plane test in adulthood as they had in adolescence. In a control experiment, adult rats were exposed to the same regimen of alcohol administration as were the adolescent animals. When these adult rats were subsequently tested, their sensitivity to alcohol-induced motor impairment was unchanged despite the repeated alcohol exposure. Thus, it is not the alcohol treatment per se that leads to reduced sensitivity to motor impairment; instead, it appears that alcohol exposure during adolescence interferes with the developmental processes that lead to adult sensitivity to alcohol's effects on motor coordination.

About the Author

NIH is the nation's medical research agency - making important medical discoveries that improve health and save lives. The National Institutes of Health (NIH), a part of the U.S. Department of Health and Human Services, is the primary Federal agency for conducting and supporting medical research.