Description:

Please join the Department of Pharmacology for a Works-in-Progress presentation by Abdelhak Belmadani and Jeffrey Calhoun.

Abdelhak Belmadani, Ph.D. - Research Assistant Professor, Miller Lab

A Role for a Newly Identified Neurogenic Niche in the Adult Brain
By Abdelhak Belmadani

Neurogenesis is known to persist in just two areas of the adult brain, the SVZ and the SGZ. Here, I will talk about a new neurogenic region (the SHZ) marked by CXCR4 receptor expression. Disruption of CXCR4 signalling or neuroinflammation leads to ectopic granule cells in the DG, some of which are derived from the SHZ. This suggest that this stem cell niche may be involved in repair of the DG and may also give rise to ectopic granule cells in the DG in the context of neuropathology associated with diseases such as epilepsy.

Jeffrey Calhoun, Ph.D. - Postdoctoral Fellow, Kearney Lab

Cacna1g is a Genetic Modifier of Epilepsy Caused by Mutation of Voltage-Gated Sodium Channel Scn2a

Mutations in neuronal voltage-gated sodium channel genes have been identified in epileptic patients. The Scn2aQ54 transgenic mouse expresses a mutant Scn2a channel which results in a strain-dependent epilepsy phenotype with recurrent focal motor seizures and reduced lifespan. Genetic mapping and RNA-Seq transcriptome analysis identified Cacna1g as a candidate modifier gene affecting Scn2aQ54 phenotype severity. We tested the effect of transgenic alteration of Cacna1g expression on the Scn2aQ54 phenotype. Scn2aQ54 mice exhibited increased spontaneous seizure frequency with elevated Cacna1g expression and decreased seizure frequency with decreased Cacna1g expression. Preliminary survival studies suggest Cacna1g as a modifier in the Scn1aKO/+ model of Dravet syndrome.