On the basis of these results and shifts of Ih channel reactivity induced by high concentrations of cAMP, Budde et al. [98] hypothesized that increased HCN1 expression in the epileptic thalamus is associated with decreased Ih channel reactivity to cAMP in thalamic neurons and leads to a loss of control over the channel, which, in turn, prolongs high Ih channel activity during absence seizures. This evidence concerns the gene HCN1 and Generalized non-motor (absence) seizure.