| pubmed-article:20113872 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:20113872 | lifeskim:mentions | umls-concept:C0205653 | lld:lifeskim |
| pubmed-article:20113872 | lifeskim:mentions | umls-concept:C0001962 | lld:lifeskim |
| pubmed-article:20113872 | lifeskim:mentions | umls-concept:C0332157 | lld:lifeskim |
| pubmed-article:20113872 | lifeskim:mentions | umls-concept:C1280500 | lld:lifeskim |
| pubmed-article:20113872 | pubmed:issue | 1 | lld:pubmed |
| pubmed-article:20113872 | pubmed:dateCreated | 2010-2-1 | lld:pubmed |
| pubmed-article:20113872 | pubmed:abstractText | This review discusses evidence for long-lasting neurophysiological changes that may occur following exposure to ethanol during adolescent development in animal models. Adolescence is the time that most individuals first experience ethanol exposure, and binge drinking is not uncommon during adolescence. If alcohol exposure is neurotoxic to the developing brain during adolescence, not unlike it is during fetal development, then understanding how ethanol affects the developing adolescent brain becomes a major public health issue. Adolescence is a critical time period when cognitive, emotional, and social maturation occurs and it is likely that ethanol exposure may affect these complex processes. To study the effects of ethanol on adolescent brain, animal models where the dose and time of exposure can be carefully controlled that closely mimic the human condition are needed. The studies reviewed provide evidence that demonstrates that relatively brief exposure to high levels of ethanol, via ethanol vapors, during a period corresponding to parts of adolescence in the rat is sufficient to cause long-lasting changes in functional brain activity. Disturbances in waking electroencephalogram and a reduction in the P3 component of the event-related potential (ERP) have been demonstrated in adult rats that were exposed to ethanol vapor during adolescence. Adolescent ethanol exposure was also found to produce long-lasting reductions in the mean duration of slow-wave sleep (SWS) episodes and the total amount of time spent in SWS, a finding consistent with a premature aging of sleep. Further studies are necessary to confirm these findings, in a range of strains, and to link those findings to the neuroanatomical and neurochemical mechanisms potentially underlying the lasting effects of adolescent ethanol exposure. | lld:pubmed |
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