Abstract
Recent findings in two rat models of absence epilepsy, the Wistar Albino Glaxo Rats from Rijswik (WAG/Rij) and the Genetic Absence Epilepsy Rats from Strasbourg (GAERS), support the idea that defects in the function of hyperpolarization-activated, cyclic nucleotide-gated cation channels (HCN1-4) and the resulting membrane current, Ih, in thalamocortical relay neurons are crucially involved in epilepsy. After a developmental evolution the expression of HCN1, which is relatively insensitive to cAMP, is elevated significantly in epileptic rats with no changes in expression of the other isoforms. This is accompanied by a hyperpolarizing shift in Ih activation and reduced sensitivity to cAMP. Thus, modification of thalamic Ih occurs at pre-epileptic stages and seems to be crucial to the development of spike-and-wave-discharges that characterize absence seizures.
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