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J Neurophysiol. 2011 Feb;105(2):528-40. doi: 10.1152/jn.00424.2010. Epub 2010 Dec 8.

Disrupted thalamic T-type Ca2+ channel expression and function during ethanol exposure and withdrawal.

Author information

1
Department of Neurobiology and Anatomy, Wake Forest University School of Medicine, Medical Center Blvd., Winston Salem, NC 27157, USA. dgodwin@wfubmc.edu

Abstract

Chronic ethanol exposure produces profound disruptions in both brain rhythms and diurnal behaviors. The thalamus has been identified as a neural pacemaker of both normal and abnormal rhythms with low-threshold, transient (T-type) Ca(2+) channels participating in this activity. We therefore examined T-type channel gene expression and physiology in the thalamus of C57Bl/6 mice during a 4-wk schedule of chronic intermittent ethanol exposures in a vapor chamber. We found that chronic ethanol disrupts the normal daily variations of both thalamic T-type channel mRNA levels and alters thalamic T-type channel gating properties. The changes measured in channel expression and function were associated with an increase in low-threshold bursts of action potentials during acute withdrawal periods. Additionally, the observed molecular and physiological alterations in the channel properties in wild-type mice occurred in parallel with a progressive disruption in the normal daily variations in theta (4-9 Hz) power recorded in the cortical electroencephalogram. Theta rhythms remained disrupted during a subsequent week of withdrawal but were restored with the T-type channel blocker ethosuximide. Our results demonstrate that a key ion channel underlying the generation of thalamic rhythms is altered during chronic ethanol exposure and withdrawal and may be a novel target in the management of abnormal network activity due to chronic alcoholism.

PMID:
21148095
PMCID:
PMC3059161
DOI:
10.1152/jn.00424.2010
[Indexed for MEDLINE]
Free PMC Article
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