Zachary Ramsey
Research Mentor: Not Available Not Available
Mentor Department: Not Available, Not Available
Author(s): Not Available
Session: Session 2 (10:00 AM – 10:50 AM)
Presentation Type: Poster 8
Abstract
CaV1.2 is a major voltage-gated L-type calcium channel encoded by the gene CACNA1C that is vital in many signaling pathways in the brain1. Extensive research exists on the relationship between GWAS-detected single-nucleotide polymorphisms detected in CACNA1C, and an increased prevalence of psychiatric disorders like major depression, schizophrenia, and bipolar disorder2,3. Additionally, it has been found the CaV1.2 channel in mice neurons is significant in processes important for fear extinction4, stress coping behaviors5, and delayed depressive-like and anxiety-like behaviors6. Furthermore, CaV1.2 channel expression is increased by chronic stress6,7 and impacted by corticosterone signaling in mice8,9,10, with Cav1.2 channel expression decreasing immediately after exposure8, but rising days after exposure9,10. However, it is not known specifically how Cav1.2 is involved in corticosterone signaling. Here we show that the general expression of the Cav1.2 channel and of associated protein subunits (notably CavB.4) in mice neurons are increased with the addition of an HA tag, while endogenous Cav1.2 from KO-Cav1.2 mice is reduced in Cre+ genotypes. In order to better understand how Cav1.2 is involved in corticosterone signaling, we want to understand if there are baseline differences in Cav1.2 subunit surface expression across genotypes and brain regions without exposure to corticosterone. We are currently investigating the regional differences of the CavB.4 subunit in Cav1.2 channels across the hippocampus, cortex, olfactory bulb, and cerebellum in these different genotypes to better understand the role CavB.4 plays in vital secondary processes like trafficking.
