Thalamic neurons undergo a shift from tonic to phasic (burst) firing upon hyperpolarization. This state transition results from deinactivaation of a regenerative depolarizing event referred to as the low-threshold spike (LTS). We have previously shown that LTS-like events can be evoked in isolated thalamic (dorsal lateral geniculate) neurons and that these potentials are mediated by a low-threshold, rapidly inactivating (T-type) calcium current. Hodgkin-Huxley modeling of the T-type calcium current indicated that the shape of the LTS can be accounted for almost entirely by the intrinsic properties of T-type calcium channels. Our model is novel in that we used two inactivation gates to account for the slow recovery from inactivation of the T-type calcium current. Burst firing in thalamic neurons mediated by the LTS is believed to be critical to the generation of absence seizures since drugs which specifically block the LTS (T-type calcium channels) prevent absence seizures. Our theoretical model of the LTS is compatible with this idea.
