Binge-Pattern Ethanol Exposure During Adolescence, but Not Adulthood, Causes Persistent Changes in GABAA Receptor-Mediated Tonic Inhibition in Dentate Granule Cells
Article first published online: 15 FEB 2013
Copyright © 2013 by the Research Society on Alcoholism
Alcoholism: Clinical and Experimental Research
Volume 37, Issue 7, pages 1154–1160, July 2013
How to Cite
Fleming, R. L., Li, Q., Risher, M.-L., Sexton, H. G., Moore, S. D., Wilson, W. A., Acheson, S. K. and Swartzwelder, H. S. (2013), Binge-Pattern Ethanol Exposure During Adolescence, but Not Adulthood, Causes Persistent Changes in GABAA Receptor-Mediated Tonic Inhibition in Dentate Granule Cells. Alcoholism: Clinical and Experimental Research, 37: 1154–1160. doi: 10.1111/acer.12087
- Issue published online: 3 JUL 2013
- Article first published online: 15 FEB 2013
- Manuscript Accepted: 29 NOV 2012
- Manuscript Received: 19 SEP 2012
- VA Career Development
- VA Merit Review
- VA Senior Research Career Scientist Awards
- NIH. Grant Number: 1U01AA019925-01
- Extrasynaptic GABAA Receptor;
- Tonic Inhibition;
- Dentate Gyrus;
In recent years, it has become clear that acute ethanol (EtOH) 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 EtOH exposure during adolescence, and most importantly whether adolescence represents a developmental period of enhanced vulnerability to such effects.
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.
CIE reduced baseline tonic current amplitude in DGGCs from animals pretreated with EtOH during adolescence, but not in GCs from those pretreated with EtOH during young adulthood or adulthood. Similarly, the enhancement of tonic currents by acute EtOH exposure ex vivo was increased in GCs from animals pretreated with EtOH during adolescence, but not in those from animals pretreated during either of the other 2 developmental periods.
These findings underscore our recent report that CIE during adolescence results in enduring alterations in tonic current and its acute EtOH sensitivity and establish that adolescence is a developmental period during which the hippocampal formation is distinctively vulnerable to long-term alteration by chronic EtOH exposure.