Kindling induces an asymmetric enhancement of N-type Ca2+ channel density in the dendritic fields of the rat hippocampus

The mechanisms underlying epilepsy are largely unknown. Recent genetic, pharmacological and electrophysiological data indicate a significant, but poorly understood, role for voltage-dependent calcium channels (VDCCs). Since the contribution of ion channels to nerve function depends on their cell surface distribution, we hypothesized that epilepsy might alter VDCC surface densities. To test this idea we mapped the expression and distribution of fluorescent-labeled hippocampal N-type VDCCs (N-VDCCs) in an animal model of epilepsy, amygdala kindling. Image analysis demonstrated that kindling induced a 21-40% increase in N-VDCC expression in CA1 but not CA3. This increase occurred in the stratum radiatum and was twice as high in tissues contra- versus ipsi-lateral to the stimulating electrode. These data rationalize recent electrophysiology and argue that a persistent alteration in N-VDCC trafficking in dendrites or nerve termini may contribute to seizure-induced synaptic plasticity.