Referenced in: none

Automatically associated channels: Cav2.3 , Slo1

Title: Cav2.3 channels are critical for oscillatory burst discharges in the reticular thalamus and absence epilepsy.

Authors: Tariq Zaman, Kyoobin Lee, Cheongdahm Park, Afshin Paydar, Jee Hyun Choi, Eunji Cheong, C Justin Lee, Hee-Sup Shin

Journal, date & volume: Neuron, 2011 Apr 14 , 70, 95-108

PubMed link: http://www.ncbi.nlm.nih.gov/pubmed/21482359

Abstract
Neurons of the reticular thalamus (RT) display oscillatory burst discharges that are believed to be critical for thalamocortical network oscillations related to absence epilepsy. Ca²+-dependent mechanisms underlie such oscillatory discharges. However, involvement of high-voltage activated (HVA) Ca²+ channels in this process has been discounted. We examined this issue closely using mice deficient for the HVA Ca(v)2.3 channels. In brain slices of Ca(v)2.3⁻/⁻, a hyperpolarizing current injection initiated a low-threshold burst of spikes in RT neurons; however, subsequent oscillatory burst discharges were severely suppressed, with a significantly reduced slow afterhyperpolarization (AHP). Consequently, the lack of Ca(v)2.3 resulted in a marked decrease in the sensitivity of the animal to γ-butyrolactone-induced absence epilepsy. Local blockade of Ca(v)2.3 channels in the RT mimicked the results of Ca(v)2.3⁻/⁻ mice. These results provide strong evidence that Ca(v)2.3 channels are critical for oscillatory burst discharges in RT neurons and for the expression of absence epilepsy.