Changes in KCNQ2 immunoreactivity in the amygdala in two rat models of temporal lobe epilepsy.

Potassium channels containing the KCNQ2 subunit play an important role in the regulation of neuronal excitability and therefore have been implicated in epilepsy. This study describes the expression of KCNQ2 subunit immunoreactivity in the basolateral amygdala in two rat models of temporal lobe epilepsy, (1) amygdala kindling and (2) spontaneously epileptic rats after status epilepticus induced by hippocampal electrical stimulation. KCNQ2 subunit immunoreactivity was assessed with a commercial antibody raised against a C-terminal part of the KCNQ2 protein. We show that KCNQ2 subunit immunoreactivity is upregulated in the basolateral amygdala in both models and that generalized seizures are required to induce this upregulation. We hypothesize that the upregulation of potassium channels containing the KCNQ2 subunit might represent a mechanism to counteract seizures in experimental temporal lobe epilepsy.