Binge-pattern ethanol exposure during adolescence, but not adulthood, causes persistent changes in GABAA receptor-mediated tonic inhibition in dentate granule cells
Background: In recent years, it has become clear that acute ethanol 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 ethanol 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 GABAA receptor-mediated tonic inhibitory currents from dentate gyrus granule cells (DGGCs) 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 DGGCs from animals pre-treated with ethanol during adolescence, but not in GCs from those pre-treated with ethanol during young adulthood or adulthood. Similarly, the enhancement of tonic currents by acute ethanol exposure ex vivo was increased in GCs from animals pre-treated with ethanol during adolescence, but not in those from animals pre-treated during either of the other two developmental periods.
Conclusions: These findings underscore our recent report that CIE during adolescence results in enduring alterations in tonic current and its acute ethanol sensitivity and establish that adolescence is a developmental period during which the hippocampal formation is distinctively vulnerable to long-term alteration by chronic ethanol exposure.
Fleming RL, Li Q, Risher ML, Sexton HG, Moore SD, Wilson WA, Acheson SK, Swartzwelder HS. Binge-pattern ethanol exposure during adolescence, but not adulthood, causes persistent changes in GABAA receptor-mediated tonic inhibition in dentate granule cells. Alcohol Clin Exp Res. 2013 Jul;37(7):1154-60. doi: 10.1111/acer.12087.