T-type Ca²⁺ currents have been proposed to be involved in the genesis of spike-and-wave discharges, a sign of absence seizures, but direct evidence in vivo to support this hypothesis has been lacking. To address this question, we generated a null mutation of the α_1G subunit of T-type Ca²⁺ channels. The thalamocortical relay neurons of the α_1G-deficient mice lacked the burst mode firing of action potentials, whereas they showed the normal pattern of tonic mode firing. The α_1G-deficient thalamus was specifically resistant to the generation of spike-and-wave discharges in response to GABA_B receptor activation. Thus, the modulation of the intrinsic firing pattern mediated by α_1G T-type Ca²⁺ channels plays a critical role in the genesis of absence seizures in the thalamocortical pathway.