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, pha rmacological and electrophysiological data indicate a significant, but poor ly understood, role for voltage-dependent calcium channels (VDCCs). Since t he contribution of ion channels to nerve function depends on their cell sur face distribution, we hypothesized that epilepsy might alter VDCC surface d ensities. To test this idea we mapped the expression and distribution of fl uorescent-labeled hippocampal N-type VDCCs (N-VDCCs) in an animal model of epilepsy, amygdala kindling. Image analysis demonstrated that kindling indu ced a 21-40% increase in N-VDCC expression in CA1 but not CA3. This increas e occurred in the stratum radiatum and was twice as high in tissues contra- versus ipsi-lateral to the stimulating electrode. These data rationalize r ecent electrophysiology and argue that a persistent alteration in N-VDCC tr afficking in dendrites or nerve termini may contribute to seizure-induced s ynaptic plasticity. (C) 1999 Elsevier Science Ireland Ltd. All rights reser ved.