In the hippocampal CA1 region in MTLE-HS, HCN1 is commonly reduced at the transcript and/or protein level, with evidence for diminished dendritic expression; in acquired post-status epilepticus models, this loss of dendritic HCN1/Ih is accompanied by a hyperpolarizing shift in Ih voltage dependence, consistent with an “acquired dendritic h-channelopathy,” which can increase CA1 pyramidal-cell responsiveness by elevating input resistance and strengthening dendritic integration (16, 76, 77). Here, HCN1 is linked to status epilepticus.