Lack of the Burst Firing of Thalamocortical Relay Neurons and Resistance to Absence Seizures

Summary T ) in thalamic neurons (Coulter etal., 1989; Kostyuk et al., 1992). In addition, T-type Ca 2 T-type Ca 2 currents have been proposed to be in- channels were moderately increased in the thalamic volved in the genesis of spike-and-wave discharges, neurons of the genetic absence epilepsy rat from Stras- a sign of absence seizures, but direct evidence in vivo bourg (GAERS), a model of spontaneous absence epi- to support this hypothesis has been lacking. To ad- lepsy (Talley et al., 2000; Tsakiridou et al., 1995). dress this question, we generated a null mutation of Results from recent studies, however, have led to the controversyabouttheroleof I T inthegenesisofabsence 1G subunit of T-type Ca 2 channels. The thalamo-cortical relay neurons of the seizures. For example, it was shown that ethosuximide 1G -deficient mice lackedthe burst mode firing of action potentials, whereas failedtosuppress I T ,butinsteadaffectedotherchannels they showed the normal pattern of tonic mode firing. such as noninactivating Na channels and Ca