Using Kcna1 null mice (Kcna1−/−), a well-known mouse model of temporal lobe epilepsy, here we show that deletion of Kv1.1 subunits alters intrinsic excitability and synaptic activity in neurons from two amygdalar subdivisions known to be involved in epilepsy and epilepsy-related comorbidities. The gene discussed is KCNA1; the disease is temporal lobe epilepsy.