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Related Experiment Videos

Nitric oxide modulates synaptic glutamate release during anoxia

A N Katchman1, N Hershkowitz

  • 1Department of Neurology, Georgetown University Medical Center, Washington, DC 20007, USA.

Neuroscience Letters
|May 30, 1997
PubMed
Summary

Nitric oxide (NO) enhances glutamate release from vesicles during oxygen deprivation (anoxia). This NO-mediated enhancement of synaptic glutamate release may contribute to excitotoxicity in hypometabolic states.

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Area of Science:

  • Neuroscience
  • Neurophysiology
  • Molecular Biology

Background:

  • Nitric oxide (NO) is a signaling molecule implicated in various physiological processes.
  • Glutamatergic neurotransmission is crucial for synaptic plasticity and function in the central nervous system.
  • Anoxia, or oxygen deprivation, can lead to altered neuronal activity and excitotoxicity.

Purpose of the Study:

  • To investigate the role of nitric oxide (NO) in modulating vesicular glutamate release during anoxia.
  • To determine the involvement of N-methyl-D-aspartate (NMDA) receptors in NO-mediated effects on synaptic transmission under anoxic conditions.

Main Methods:

  • Whole-cell patch clamp recordings were performed on CA1 pyramidal neurons in rat hippocampal slices.
  • Tetrodotoxin was used to isolate spontaneous glutamatergic miniature excitatory postsynaptic currents (mEPSCs).

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  • The effects of NO-synthase inhibitors, reduced hemoglobin, NMDA receptor antagonists, and arginine were assessed during anoxia.

    • Main Results:

    • Anoxia exposure increased the frequency of mEPSCs in CA1 pyramidal neurons.
    • Inhibition of NO production (using NO-synthase inhibitors or reduced hemoglobin) attenuated the anoxia-induced increase in mEPSC frequency.
    • NMDA receptor antagonists also suppressed the anoxia-induced increase in mEPSC frequency.
    • Supplementation with arginine reversed the inhibitory effects of NO-synthase inhibitors.

    Conclusions:

    • NMDA receptor activation leads to NO production, which enhances vesicular synaptic glutamate release during anoxia.
    • This NO-mediated enhancement of glutamate release may contribute to excitotoxicity during hypometabolic states such as stroke or cardiac arrest.