Referenced in: none

Automatically associated channels: TRP , TRPM , TRPM2 , TRPM7

Title: Non-NMDAR neuronal Ca(2+)-permeable channels in delayed neuronal death and as potential therapeutic targets for ischemic brain damage.

Authors: Chaokun Li, Li Meng, Xin Li, Dongliang Li, Lin-Hua Jiang

Journal, date & volume: Expert Opin. Ther. Targets, 2015 Mar 2 , , 1-14

PubMed link: http://www.ncbi.nlm.nih.gov/pubmed/25732672

Abstract
Transient cerebral ischemia represents the most common cause of complex chronic disability in adults due to delayed neuronal death as a result of aberrant post-ischemic increases in the [Ca(2+)]c and [Zn(2+)]c. A number of Ca(2+)-permeable channels are engaged in transient ischemia-induced neuronal death.In this review, the authors discuss the GluA2-lacking AMPARs, acid-sensing ion channel 1a, melastatin-related transient receptor potential 2 (TRPM2), TRPM7 and store-operated Ca(2+) channels expressed in ischemia-vulnerable neurons, and focus on the studies using in vitro and in vivo models of transient ischemia that supports a significant role for these channels in inducing increases in the [Ca(2+)]c and/or [Zn(2+)]c and delayed neuronal death, and their potential as therapeutic targets.Non-NMDAR Ca(2+)-permeable channels are important mechanisms mediating delayed neuronal death and cognitive dysfunctions after transient ischemia. Identification of such Ca(2+)-permeable channels significantly improves our understanding of the molecular events leading to ischemic brain damage and provides promising novel targets for post-ischemic therapeutics treating ischemic brain damage.