Chronic alcohol abuse depresses the nervous system and, upon cessation, rebound 
hyperexcitability can result in withdrawal seizure. Withdrawal symptoms, 
including seizures, may drive individuals to relapse, thus representing a 
significant barrier to recovery. Our lab previously identified an upregulation 
of the thalamic T-type calcium (T channel) isoform CaV3.2 as a potential 
contributor to the generation and propagation of seizures in a model of 
withdrawal. In the present study, we examined whether ethosuximide (ETX), a 
T-channel antagonist, could decrease the severity of ethanol withdrawal seizures 
by evaluating electrographical and behavioral correlates of seizure activity. 
DBA/2J mice were exposed to an intermittent ethanol exposure paradigm. Mice were 
treated with saline or ETX in each withdrawal period, and cortical EEG activity 
was recorded to determine seizure severity. We observed a progression in seizure 
activity with each successive withdrawal period. Treatment with ETX reduced 
ethanol withdrawal-induced spike and wave discharges (SWDs), in terms of 
absolute number, duration of events, and contribution to EEG power in the 6-10 
Hz frequency range. We also evaluated the effects of ETX on handling-induced 
convulsions. Overall, we observed a decrease in handling-induced convulsion 
severity in mice treated with ETX. Our findings suggest that ETX may be a useful 
pharmacological agent for studies of alcohol withdrawal and treatment of 
resulting seizures.