Targeting protein phosphatase 2A (PP2A) activity to mitigate electrophysiological deficits due to blast-induced traumatic brain injury
We are sorry, this position has been filled.
Previous studies have suggested that traumatic brain injury (TBI) decreases protein phosphatase 2A (PP2A) activity and this leads to electrophysiological deficits. In vivo administration of sodium selenate has been shown to increase PP2A activity and improve cognitive function. Our goal is to treat rat organotypic hippocampal slice cultures exposed to blats-induced TBI with sodium selenate and identify a range of nontoxic concentrations of this drug to use in electrophysiology experiments.
Lab: Neurotrauma and Repair Laboratory, Barclay Morrison