Ca_V 3.2 drives sustained burst-firing, which is critical for absence seizure propagation in reticular thalamic neurons.

ABSTRACT:

Objective

Genetic alterations have been identified in the CACNA1H gene, encoding the Ca_V 3.2 T-type calcium channel in patients with absence epilepsy, yet the precise mechanisms relating to seizure propagation and spike-wave-discharge (SWD) pacemaking remain unknown. Neurons of the thalamic reticular nucleus (TRN) express high levels of Ca_V 3.2 calcium channels, and we investigated whether a gain-of-function mutation in the Cacna1h gene in Genetic Absence Epilepsy Rats from Strasbourg (GAERS) contributes to seizure propagation and pacemaking in the TRN.

Methods

Pathophysiological contributions of Ca_V 3.2 calcium channels to burst firing and absence seizures were assessed in vitro using acute brain slice electrophysiology and quantitative real

SUBMITTER: Cain SM 

PROVIDER: S-EPMC5900875 | biostudies-literature | 2018 Apr

REPOSITORIES: biostudies-literature