Disruption of IP3R2-mediated Ca(2+) signaling pathway in astrocytes ameliorates neuronal death and brain damage while reducing behavioral deficits after focal ischemic stroke.

Disruption of IP3R2-mediated Ca(2+) signaling pathway in astrocytes ameliorates neuronal death and brain damage while reducing behavioral deficits after focal ischemic stroke. Cell Calcium. 2015 Sep 25; Authors: Li H, Xie Y, Zhang N, Yu Y, Zhang Q, Ding S Abstract Inositol trisphosphate receptor (IP3R)-mediated intracellular Ca(2+) increase is the major Ca(2+) signaling pathway in astrocytes in the central nervous system (CNS). Ca(2+) increases in astrocytes have been found to modulate neuronal function through gliotransmitter release. We previously demonstrated that astrocytes exhibit enhanced Ca(2+) signaling in vivo after photothrombosis (PT)-induced ischemia, which is largely due to the activation of G-protein coupled receptors (GPCRs). The aim of this study is to investigate the role of astrocytic IP3R-mediated Ca(2+) signaling in neuronal death, brain damage and behavior outcomes after PT. For this purpose, we conducted experiments using homozygous type 2 IP3R (IP3R2) knockout (KO) mice. Histological and immunostaining studies showed that IP3R2 KO mice were indeed deficient in IP3R2 in astrocytes and exhibited normal brain cytoarchitecture. IP3R2 KO mice also had the same densities of S100β+ astrocytes and NeuN+ neurons in the cortices, and exhibited the same glial fibrillary acidic protein (GFAP) and glial glutamate transporter (GLT-1) levels in the cortices and hippocampi as compared with wild type (WT) mice. Two-photon (2-P...
Source: Cell Calcium - Category: Cytology Authors: Tags: Cell Calcium Source Type: research