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.