GluR3B Ab's induced oligodendrocyte precursor cells excitotoxicity via mitochondrial dysfunction.

In this study, we found that the survival rate of OPCs decreased, apoptosis increased and the release of LDH increased with GluR3B Ab's treatment. GluR3B Ab's enhanced the level of intracellular Ca(2+) and reactive oxygen species (ROS), caused mitochondrial potential collapse measured by JC-1 and promoted mitochondrial cytochrome C release. AMPARs antagonist NBQX reversed OPCs apoptosis caused by GluR3B Ab's. Taken together, these data suggests that AMPAR was involved in GluR3B Ab's-induced OPCs toxicity by mitochondrial dysfunction. The study revealed a new mechanism for OPCs excitotoxicity in many central nervous system diseases such as epilepsy. PMID: 28063880 [PubMed - as supplied by publisher]

https://www.ncbi.nlm.nih.gov/pubmed/28063880?dopt=Abstract

Source: Brain Research Bulletin - January 3, 2017 Category: Neurology Authors: Liu Y, Chen Y, Du WT, Wu XX, Dong FX, Qu XB, Fan HB, Yao RQ Tags: Brain Res Bull Source Type: research