Binge‐Pattern Ethanol Exposure During Adolescence, but Not Adulthood, Causes Persistent Changes in GABA A Receptor‐Mediated Tonic Inhibition in Dentate Granule Cells

Background In recent years, it has become clear that acute ethanol ( E t OH ) affects various neurobiological and behavioral functions differently in adolescent animals than in adults. However, less is known about the long‐term neural consequences of chronic E t OH exposure during adolescence, and most importantly whether adolescence represents a developmental period of enhanced vulnerability to such effects. Methods We made whole‐cell recordings of GABA A receptor‐mediated tonic inhibitory currents from dentate gyrus granule cells ( DGGC s) in hippocampal slices from adult rats that had been treated with chronic intermittent ethanol ( CIE ) or saline during adolescence, young adulthood, or adulthood. Results CIE reduced baseline tonic current amplitude in DGGC s from animals pretreated with E t OH during adolescence, but not in GC s from those pretreated with E t OH during young adulthood or adulthood. Similarly, the enhancement of tonic currents by acute E t OH exposure ex vivo was increased in GC s from animals pretreated with E t OH during adolescence, but not in those from animals pretreated during either of the other 2 developmental periods. Conclusions These findings underscore our recent report that CIE during adolescence results in enduring alterations in tonic current and its acute E t OH sensitivity and establish that adolescence is a developmental period during which the hippocampal formation is distinctively vulnerable to long‐term alteration by chronic E t OH exposure.