Date: 14 Feb 2012

Voltage-Gated Ca2+ Channel Mediated Ca2+ Influx in Epileptogenesis

* Final gross prices may vary according to local VAT.

Get Access

Abstract

Voltage- and ligand-gated ion channels are key elements in the etiopathogenesis of various forms of epilepsy. In this chapter, we present an overview of the functional implications of voltage-gated Ca2+ channels in modulating internal Ca2+ level fluctuations and generating ictiform/epileptiform cellular electrophysiological activity. A specific focus will be on the fascinating and evolving field of high-voltage activated (HVA) Non-L-type Cav2.3 R-type channels and low-voltage activated (LVA) Cav3.1–3.3 T-type Ca2+ channels in the genesis of plateau potentials and excessive rebound bursting. Plateau potentials have been characterised in the hippocampus and were shown to be triggered by Cav2.3 which subsequently activate CNG channels that mediate long-lasting plateaus. In the thalamocortical network, a complex ion channel armamentarium is involved in regulating a complex balance of burst and tonic mode activity. Recent findings point to an outstanding role of R- and T-type channels in both thalamocortical eurhythmia and pathophysiological ­aberrations. Thus, pharmacological modulation of voltage-gated Ca2+-channels might prove more and more important in treatment of neurological and psychiatric disorder such as schizophrenia, mania, dementia and epilepsy.