The T-type Ca2+ channels critically contribute to the generation of rhythmic burst activity in the thalamocortical system during states of slow wave sleep and absence epilepsy, but the correlation between T-type Ca2+ channel expression and cellular output pattern have not been fully determined. We examined T- currents and related properties in the thalamus of a rat model of absence epilepsy, the WAG/Rij rats and a non-epileptic control strain, the ACI rats. Two relay nuclei, the dorsal lateral geniculate nucleus (LGN) and the centrolateral nucleus (CL), as well as the GABAergic reticular nucleus of the thalamus (NRT) have been investigated. We correlated the expression of the three known T- channel coding genes (CACNA1G, -H, -I) with isolated T- currents in brain slice preparations and the low threshold Ca2+ spike (LTS). Both relay nuclei were found to primarily express CACNA1G, while the NRT primarily expressed CACNA1H and - I. Expression levels were significantly increased in WAG/Rij rats. The T-current densities and steady-state T-current voltage dependencies were different between nuclei and epileptic and non- epileptic rats. The LTS, the main voltage expression of T-channel activation, differed qualitatively between nuclei, but not between stains. A quantification of LTS parameters revealed a clear difference between the relay nuclei and the NRT in both strains, but only subtle differences between WAG/Rij and ACI rats.