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Chronic Intermittent Ethanol Vapor Exposure Paired with Two-Bottle Choice to Model Alcohol Use Disorder

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

J D Graef¹, T W Huitt, B K Nordskog

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

Journal of Neurophysiology

|December 15, 2010

Summary

Chronic ethanol exposure alters thalamic T-type calcium channels, disrupting brain rhythms and daily behaviors. Ethosuximide restored disrupted theta rhythms, suggesting T-type channels as a target for alcoholism-related neurological issues.

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Area of Science:

Neuroscience
Pharmacology
Molecular Biology

Background:

Chronic ethanol exposure significantly disrupts brain rhythms and diurnal behaviors.
The thalamus acts as a neural pacemaker, with T-type calcium channels crucial for rhythm generation.
Understanding ethanol's impact on thalamic function is vital for addressing alcohol-related neurological disorders.

Purpose of the Study:

To investigate the effects of chronic ethanol exposure on T-type calcium channel gene expression and physiology in the mouse thalamus.
To correlate molecular and physiological changes in T-type channels with disruptions in brain rhythms during ethanol withdrawal.
To assess the potential of T-type channel blockers in mitigating ethanol-induced rhythm abnormalities.

Main Methods:

Chronic intermittent ethanol exposure in C57Bl/6 mice using a vapor chamber for 4 weeks.
Analysis of T-type calcium channel mRNA levels and gating properties in the thalamus.
Electrophysiological recordings of cortical electroencephalogram (EEG) to measure theta power (4-9 Hz).
Administration of ethosuximide, a T-type channel blocker, during withdrawal.

Main Results:

Chronic ethanol exposure altered daily variations in thalamic T-type channel mRNA and gating properties.
Observed molecular and physiological changes correlated with increased low-threshold action potential bursts during withdrawal.
Disrupted diurnal variations in cortical theta power during withdrawal were restored by ethosuximide treatment.

Conclusions:

Chronic ethanol exposure alters a key ion channel (T-type calcium channels) involved in thalamic rhythm generation.
These alterations contribute to abnormal network activity and disrupted brain rhythms during ethanol withdrawal.
T-type calcium channels represent a potential novel therapeutic target for managing neurological complications of chronic alcoholism.