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Related Experiment Videos

Nitric oxide causes glutamate release from brain synaptosomes

K S McNaught1, G C Brown

  • 1Department of Biochemistry, University of Cambridge, England, UK.

Journal of Neurochemistry
|April 2, 1998
PubMed
Summary

Pathological levels of nitric oxide (NO) trigger calcium-independent glutamate release from rat brain nerve terminals by inhibiting mitochondrial respiration. This suggests NO-induced mitochondrial dysfunction contributes to excitotoxicity and neuronal death in neurological diseases.

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Area of Science:

  • Neuroscience
  • Biochemistry
  • Cell Biology

Background:

  • Nitric oxide (NO) plays complex roles in the central nervous system.
  • Pathological levels of NO are implicated in neurodegenerative processes.

Purpose of the Study:

  • To investigate the mechanism by which nitric oxide (NO) induces glutamate release from isolated rat brain nerve terminals.
  • To determine if NO-induced glutamate release is linked to mitochondrial dysfunction.

Main Methods:

  • Utilized a fluorometric assay to measure glutamate release from isolated rat brain synaptosomes.
  • Administered varying concentrations of NO and NO-releasing compounds.
  • Assessed the impact of inhibitors of soluble guanylyl cyclase and mitochondrial respiration.
  • Measured synaptosomal respiration rates under different conditions.

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Main Results:

  • Pathological levels of NO (0.7 and 2 microM) induced significant Ca2+-independent glutamate release.
  • NO, spermine NONOate (a slow NO donor), and potassium cyanide (cytochrome oxidase inhibitor) all caused Ca2+-independent glutamate release.
  • NO-induced glutamate release was enhanced in low-oxygen conditions.
  • NO and cyanide inhibited synaptosomal respiration, correlating with glutamate release potency.
  • Inhibition of soluble guanylyl cyclase did not affect NO-induced glutamate release.

Conclusions:

  • Nitric oxide induces Ca2+-independent glutamate release by inhibiting mitochondrial respiration at the level of cytochrome oxidase.
  • NO-induced mitochondrial dysfunction, leading to glutamate release and excitotoxicity, may contribute to neuronal death in neurological diseases.
  • These findings highlight a novel pathway for NO-mediated neurotoxicity.