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Non-NMDAR neuronal Ca(2+)-permeable channels in delayed neuronal death and as potential therapeutic targets for

Chaokun Li1, Li Meng, Xin Li

  • 1Xinxiang Medical University, School of Basic Medical Sciences, Department of Physiology and Neurobiology , Xinxiang , China.

Expert Opinion on Therapeutic Targets
|March 4, 2015
PubMed
Abstract

Insights

Non-NMDAR calcium-permeable channels contribute to delayed neuronal death after transient cerebral ischemia. Targeting these channels offers potential therapeutic strategies for ischemic brain damage and cognitive dysfunction.

Area of Science:

  • Neuroscience
  • Cell Biology
  • Pharmacology

Background:

  • Transient cerebral ischemia is a leading cause of adult disability.
  • Delayed neuronal death results from abnormal intracellular calcium ([Ca(2+)]c) and zinc ([Zn(2+)]c) increases.
  • Specific ion channels are implicated in ischemia-induced neuronal death.

Purpose of the Study:

  • To review the role of non-NMDA receptor (non-NMDAR) calcium-permeable channels in transient ischemia.
  • To highlight the potential of these channels as therapeutic targets for ischemic brain damage.

Main Methods:

  • Review of in vitro and in vivo studies on transient ischemia models.
  • Focus on GluA2-lacking AMPARs, acid-sensing ion channel 1a, TRPM2, TRPM7, and store-operated Ca(2+) channels.
  • Analysis of their role in [Ca(2+)]c and [Zn(2+)]c regulation and neuronal death.

Main Results:

  • Non-NMDAR Ca(2+)-permeable channels significantly contribute to increased intracellular calcium and zinc.
  • These channels play a critical role in delayed neuronal death following transient ischemia.
  • Evidence supports their involvement in ischemia-induced cognitive dysfunctions.

Conclusions:

  • Non-NMDAR Ca(2+)-permeable channels are key mediators of delayed neuronal death and cognitive deficits post-ischemia.
  • Understanding these channels enhances knowledge of ischemic brain damage mechanisms.
  • These channels represent promising therapeutic targets for treating ischemic brain injury.
Keywords:
AMPARsCa2+Zn2+acid-sensing ion channel 1adelayed neuronal deathmelastatin-related transient receptor potential 2melastatin-related transient receptor potential 7store-operated Ca2+ channelstransient ischemia

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