The role of T-type calcium channel genes in absence seizures.

Yucai Chen,Keling Wang,William Davis Parker

doi:10.3389/fneur.2014.00045

Abstract

The thalamic relay neurons, reticular thalamic nucleus, and neocortical pyramidal cells form a circuit that sustains oscillatory burst firing, and is regarded as the underlying mechanism of absence seizures. T-type calcium channels play a key role in this circuit. Here, we review the role of T-type calcium channel genes in the development of absence seizures, and emphasize gain or loss of function mutations, and other variations that alter both quantity and quality of transcripts, and methylation status of isoforms of T-type calcium channel proteins might be of equal importance in understanding the pathological mechanism of absence seizures.

Highlights

Genetic generalized epilepsies (GGE) are regarded as primarily GGE, which are frequently expressed sporadically in a population
Different T-type calcium channel genes are coexpressed in a single neuron, e.g., Cav3.2 and Cav3.3 are coexpressed in reticular thalamic nucleus (RT) neurons, where they are thought to be responsible for generating the slow wave discharges (SWD) seen in absence epilepsy
Due to the highly complex and widespread effects of different channel genes involved in this circuit, even small alterations in their expression www.frontiersin.org or biophysical properties can induce pathophysiological changes in the brain with the potential to induce epileptic seizures [7]

Summary

Introduction

Genetic generalized epilepsies (GGE) are regarded as primarily GGE, which are frequently expressed sporadically in a population. Different T-type calcium channel genes are coexpressed in a single neuron, e.g., Cav3.2 and Cav3.3 are coexpressed in RT neurons, where they are thought to be responsible for generating the SWD seen in absence epilepsy.

Results

Conclusion