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Alteration of neuronal calcium homeostasis and excitotoxic vulnerability by chronic depolarization

M Tymianski1, L Y Wang, J F MacDonald

  • 1Playfair Neuroscience Unit, Toronto Hospital, Ont., Canada.

Brain Research
|June 20, 1994
PubMed

Insights

Neurons cultured in high potassium showed reduced calcium responses and better survival against excitotoxins like NMDA. This suggests altered intracellular calcium handling offers neuroprotection.

Area of Science:

  • Neuroscience
  • Cellular Biology
  • Neurophysiology

Background:

  • Excitatory amino acids (EAAs) like NMDA and kainate can cause neuronal damage.
  • Intracellular calcium regulation is crucial for neuronal function and survival.

Purpose of the Study:

  • To investigate the effect of chronic depolarization on neuronal response to EAAs.
  • To explore potential neuroprotective mechanisms against excitotoxicity.

Main Methods:

  • Studied spinal neurons cultured in low (4.5 mM) and high (25 mM) extracellular potassium.
  • Measured free intracellular calcium concentration ([Ca2+]i) and calcium currents.
  • Assessed excitatory amino acid (EAA) currents and neuronal survival after NMDA or kainate challenge.

Main Results:

  • Neurons in high potassium (25 mM K+) exhibited attenuated Ca2+ currents and [Ca2+]i responses to NMDA and kainate.
  • These neurons showed enhanced survival rates when challenged with lethal EAA concentrations.
  • NMDA and kainate currents were comparable between high- and low-potassium-cultured neurons, indicating altered intracellular calcium handling.

Conclusions:

  • Chronic depolarization fundamentally alters intracellular calcium handling in neurons.
  • This alteration confers significant neuroprotection against excitotoxic challenges.
  • Findings may inform the development of neuroprotective strategies against excitotoxin-induced neuronal damage.

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