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Related Experiment Videos

Modulation of spreading depression by changes in extracellular pH.

C K Tong1, M Chesler

  • 1Department of Physiology and Neuroscience and Department of Neurosurgery, New York University School of Medicine, New York, New York 10016, USA.

Journal of Neurophysiology
|November 9, 2000
PubMed
Summary

Acidosis inhibits spreading depression (SD) by increasing induction thresholds and slowing propagation. However, an alkaline shift can overcome this inhibition, potentially contributing to NMDA receptor-mediated injury during ischemia.

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Area of Science:

  • Neuroscience
  • Physiology

Background:

  • Spreading depression (SD) is linked to hypoxic-ischemic injury.
  • SD occurs during marked extracellular acidosis and can cause pH shifts.

Purpose of the Study:

  • Investigate interstitial acidosis effects on SD generation and propagation in hippocampal slices.
  • Examine the role of alkaline shifts in modulating SD using a carbonic anhydrase inhibitor.

Main Methods:

  • Manipulated extracellular pH (pHo) using varying HCO3- and CO2 concentrations.
  • Recorded pHo with microelectrodes and monitored SD parameters (induction, velocity, duration).
  • Utilized benzolamide to inhibit carbonic anhydrase and amplify alkaline shifts; tested NMDA receptor antagonist.

Main Results:

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  • Acidosis increased SD induction threshold, decreased velocity, and shortened duration, with maximal inhibition at lowest pHo.
  • Benzolamide amplified the early alkaline shift, increasing SD duration and velocity, especially in acidic conditions.
  • Amplified alkalosis prolonged [Ca2+]o transients; this augmentation was blocked by NMDA receptor antagonist.

Conclusions:

  • A fall in baseline pH inhibits SD induction and propagation, characteristic of ischemic conditions.
  • The early alkaline shift can counteract acidosis-induced inhibition by relieving proton block on NMDA receptors.
  • Intrinsic alkalosis during ischemia may facilitate SD, contributing to NMDA receptor-mediated injury.