Alcohol Effects on Brain : Adolescents, Part 3

by National Institute of Health

(Page 6 of 6)

In a similar experiment, White and colleagues evaluated how chronic intermittent alcohol exposure during adolescence affects rats' spatial memory in adulthood. As discussed earlier, acute alcohol administration impairs learning and memory more in adolescent animals than it does in adults. For this experiment, adolescent and adult animals were repeatedly exposed to high doses of alcohol. When all the animals had reached adulthood, the investigators compared their ability to learn where to retrieve food in a maze with that of animals which had never received alcohol. They found that animals in all test groups (i.e., with or without alcohol administration during adolescence or adulthood) learned to perform the memory task equally well. However, when the animals received a low dose of alcohol just before being tested on the memory task, those that had been exposed to alcohol as adolescents performed worse than animals in the other three groups. These results indicate that repeated alcohol exposure during adolescence enhances the individual's sensitivity to alcohol's memory-impairing effects during adulthood. Similar results were obtained in a study of college students, which found that students with a history of binge drinking performed worse on memory tasks after consuming alcohol than did students without such a history.

Researchers also have demonstrated the long-term consequences of adolescent alcohol exposure on adult brain function by measuring the electrical brain activity of adult rats that had or had not been repeatedly exposed to alcohol during adolescence. Using electrodes implanted in various regions of the animals' brains, researchers examined both the electroencephalogram, which is a measure of ongoing brain activity, and event-related potentials, which are spikes in brain activity induced by a sudden stimulus. One of the studies found that animals which had been exposed to alcohol during adolescence showed changes in the EEG pattern as well as in ERPs measured in various brain regions, particularly the hippocampus. These investigators noted that although similar effects have been reported following long-term alcohol exposure during adulthood, alcohol exposure during adolescence appears to result in more stable effects, especially on the hippocampus, after shorter periods of exposure than would be observed in adult animals.

Similar experiments have examined the effects of an acute alcohol dose on the EEG of adult rats that had or had not been exposed to alcohol repeatedly during adolescence. A study by Slawecki found that although the acute alcohol dose significantly altered several EEG variables in the hippocampus and other brain regions of the control animals, these variables were not altered in the animals that had been exposed to alcohol during adolescence. In addition, the alcohol-exposed animals showed fewer behaviors indicative of intoxication in response to the acute alcohol dose than did the control animals. These findings suggest that alcohol exposure during adolescence leads to persistent and brain region-specific changes in electrical brain activity in response to an acute alcohol dose during adulthood. In particular, the observation that some EEG responses to alcohol were reduced in the alcohol-exposed animals indicates that adolescent alcohol exposure can produce long-lasting changes in responsiveness to at least some alcohol effects.

Conclusions

Various avenues of research have demonstrated that at least in laboratory animals, adolescence is a unique stage of brain development which is particularly sensitive to the disrupting effects of alcohol. For example, in rodents, adolescent alcohol exposure increases the brain's sensitivity to some alcohol effects (e.g., memory impairment) and decreases sensitivity to other effects (e.g., motor impairment and sedation). Furthermore, in rodents, alcohol exposure during adolescence not only has an immediate impact on brain function, it also may lead to consequences for various brain functions that last even into adulthood. To what extent these findings are applicable to humans is a matter of debate, particularly because of the differences between humans and rodents in terms of the plasticity and time course of brain development. Nevertheless these findings suggest that similar processes might occur in humans - a conclusion that is especially pertinent and worrisome because adolescence in humans often is the period when alcohol consumption begins and when particularly dangerous drinking patterns, such as binge drinking, are common. This combination of frequent high alcohol consumption and increased vulnerability of the brain to alcohol's harmful effects may result in cognitive deficits and other problems that persist far beyond adolescence.

One brain area that seems to be particularly affected by adolescent alcohol consumption is the hippocampus, which plays a role in numerous cognitive functions, including learning and memory. In fact, preliminary studies in humans have found that alcohol abuse during adolescence may be associated with a reduction in the size of the hippocampus, which in turn could be a sign of impaired hippocampal function. Theoretically, alcohol could lead to cell death in the hippocampus through several mechanisms (e.g., by excessive activation of the glutamate/NMDA receptor system). Several studies, however, have failed to detect obvious nerve cell loss after repeated exposure to various patterns of alcohol administration during adolescence or early adulthood. Other studies, in contrast, have found that high-dose binge exposure to alcohol led to brain damage in adolescents but not in adults. These differences in findings may be accounted for by differences in the rodent strain used; in the pattern, dose, and route of alcohol administration; and in the brain regions studied. In addition, the long-term behavioral changes that follow chronic intermittent alcohol exposure during adolescence may involve subtle changes in neuronal connections which are not easily measurable. Thus, additional research is necessary to elucidate the exact effects of alcohol on the adolescent hippocampus and other brain structures and to better understand the long-term implications of adolescent alcohol exposure.

About the Author

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