Ethanol consumption by juveniles and adolescents is a public health problem of massive proportions. Recent studies have indicated that adolescents may be less sedated by ethanol than adults, and may thus be able to consume more ethanol, putting them at greater risk for ethanol addiction and other negative consequences of ethanol use. However, the mechanisms underlying this developmental difference are unknown. One contributing factor may be GABAA receptor-mediated inhibition, which is known to produce sedation. Ethanol is known to enhance this inhibitory process. Using whole cell recording, we tested the response of GABAA receptor-mediated IPSCs in brain slices of rat hippocampus from animals representing three developmental stages: juvenile, early adolescent, and adult. We found significantly greater ethanol-induced enhancement of GABA-mediated IPSPs in cells from adult animals compared to those from juvenile or adolescent animals. We conclude that the sensitivity of GABAA receptor-mediated inhibitory processes to ethanol increases with development from the juvenile period to adulthood.
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