Non-NMDAR neuronal Ca2+–permeable channels in delayed neuronal death and as potential therapeutic targets for ischemic brain damage. (July 2015)

• Record Type: Journal Article
• Authors: Li, Chaokun; Meng, Li; Li, Xin; Li, Dongliang; Jiang, Lin-Hua
• Is Part Of: Expert opinion on therapeutic targets. Volume 19:Number 7(2015:Jul.)
• Page Start: 879
• Page End: 892
• Publication Date: 2015-07
• Subjects: Drugs -- Research -- Periodicals; 615.072
• DOI: 10.1517/14728222.2015.1021781
• Languages: English
• ISSNs: 1744-7631

Abstract

<abstract> <title> <x xml:space="preserve">Abstract</x> </title> <p> <bold> <italic>Introduction:</italic> </bold> 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<sup>2+</sup>]<sub>c</sub> and [Zn<sup>2+</sup>]<sub>c</sub>. A number of Ca<sup>2+</sup>-permeable channels are engaged in transient ischemia-induced neuronal death.</p> <p> <bold> <italic>Areas covered:</italic> </bold> 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<sup>2+</sup> channels expressed in ischemia-vulnerable neurons, and focus on the studies using <italic>in vitro</italic> and <italic>in vivo</italic> models of transient ischemia that supports a significant role for these channels in inducing increases in the [Ca<sup>2+</sup>]<sub>c</sub> and/or [Zn<sup>2+</sup>]<sub>c</sub> and delayed neuronal death, and their potential as therapeutic targets.</p> <p> <bold> <italic>Expert opinion:</italic> </bold> Non-NMDAR Ca<sup>2+</sup>-permeable channels are important mechanisms mediating delayed neuronal death and cognitive dysfunctions after transient ischemia. Identification of such Ca<sup>2+</sup>-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.</p> </abstract>