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Related Experiment Videos

Acid sensing ionic channels: modulation by redox reagents.

Fedorenko Andrey1, Timur Tsintsadze, Tatyana Volkova

  • 1Department of Cellular Membranology, Bogomoletz Institute of Physiology, Kiev, Ukraine.

Biochimica Et Biophysica Acta
|August 9, 2005
PubMed
Summary
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Acid-sensing ion channels (ASICs) are modulated by redox agents. Reducing agents like dithiothreitol (DTT) and glutathione (GSH) potentiate proton-activated currents, while oxidizing agents inhibit them.

Area of Science:

  • Neuroscience
  • Ion Channel Physiology
  • Redox Biology

Background:

  • Acid-sensing ion channels (ASICs) are crucial for sensory neuron function, particularly in nociception.
  • Tissue redox status fluctuates during physiological processes, potentially impacting neuronal function.
  • ASICs' role in acid sensing and pain suggests their activity may be influenced by cellular redox environment.

Purpose of the Study:

  • To investigate the effect of redox reagents on ASIC-like currents in rat sensory ganglia and hippocampal neurons.
  • To determine if reducing or oxidizing agents alter the function of proton-activated ion channels.
  • To explore the potential redox modulation of ASIC activity.

Main Methods:

  • Whole-cell patch-clamp recordings.

Related Experiment Videos

  • Concentration clamp techniques.
  • Application of redox reagents (DTT, DTNB, GSH) to neurons.

    • Main Results:

    • Dithiothreitol (DTT) and glutathione (GSH) reversibly potentiated proton-activated currents.
    • 5,5'-dithio-bis-(2-nitrobenzoic acid) (DTNB) inhibited these currents.
    • Redox modulation was independent of membrane potential and pH activation levels.
    • EC50 and Hill coefficient for proton activation remained unaffected by DTT.

    Conclusions:

    • ASIC-like currents are sensitive to redox regulation.
    • Reducing agents enhance ASIC activity, while oxidizing agents inhibit it.
    • This suggests a novel mechanism for modulating neuronal excitability and acid sensing via redox control.