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Related Experiment Videos

Acidotoxicity in brain ischaemia.

R Simon1, Z Xiong

  • 1Legacy Clinical Research and Technology Center, 1225 NE 2nd Avenue, Portland, OR 97232, USA. rsimon@downeurobiology.org

Biochemical Society Transactions
|November 1, 2006
PubMed
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Acid-sensing ion channels (ASICs) offer a new target for stroke therapy. Blocking ASICs reduces calcium toxicity and brain damage during ischaemia, providing a potential treatment for stroke.

Area of Science:

  • Neuroscience
  • Pathophysiology
  • Pharmacology

Background:

  • Intracellular calcium toxicity is central to ischaemic brain injury.
  • Glutamate-gated channels were presumed major calcium entry sites, but clinical trials failed.
  • Glutamate-independent mechanisms of calcium entry are critical in ischaemia.

Purpose of the Study:

  • Investigate acid-sensing ion channels (ASICs) as glutamate-independent calcium entry pathways in brain ischaemia.
  • Determine if ASICs contribute to calcium toxicity during acidosis and substrate depletion.
  • Evaluate pharmacological blockade of ASICs as a potential stroke therapy.

Main Methods:

  • Utilized in vitro and in vivo models of brain ischaemia.
  • Assessed calcium flux through ASICs under ischaemic conditions (acidosis, substrate depletion).

Related Experiment Videos

  • Administered ASIC blockers to evaluate their effect on stroke injury.

    • Main Results:

    • ASICs function as glutamate-independent calcium channels in the brain.
    • ASICs transport significant calcium during acidosis and substrate depletion.
    • Pharmacological blockade of ASICs substantially reduced stroke injury.
    • A therapeutic window of 5 hours was observed for ASIC blockade post-stroke.

    Conclusions:

    • ASICs represent a novel mechanism of calcium toxicity in brain ischaemia.
    • Targeting ASICs offers a promising therapeutic strategy for stroke.
    • ASIC blockade demonstrates a significant therapeutic potential with a notable time window.