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Nitric oxide in the central nervous system

S A Lipton1, D J Singel, J S Stamler

  • 1Department of Neurology, Harvard Medical School, Boston, MA 02115.

Progress in Brain Research
|January 1, 1994
PubMed
Summary

Nitric oxide (NO) can be neurotoxic or neuroprotective depending on its chemical form and the cellular redox environment. Protein S-nitrosylation offers potential therapeutic strategies for neurological disorders.

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Area of Science:

  • Neuroscience
  • Biochemistry
  • Pharmacology

Background:

  • Nitric oxide (NO) plays a dual role in neurotoxicity and neuroprotection.
  • The formation of peroxynitrite from NO and superoxide contributes to neurotoxicity.
  • Protein S-nitrosylation is a key mechanism regulating cell function and signaling.

Purpose of the Study:

  • To elucidate the distinct neurotoxic and neuroprotective pathways of nitric oxide.
  • To investigate the role of protein S-nitrosylation in modulating NMDA receptor activity.
  • To explore novel therapeutic strategies targeting NO-mediated pathways in neurological disorders.

Main Methods:

  • Analysis of nitric oxide reactions with superoxide.
  • Investigation of NO+ group transfer to NMDA receptor thiols.
  • Assessment of the influence of local redox milieu on NO signaling.

Main Results:

  • Neurotoxicity arises from peroxynitrite formation, not NO alone.
  • S-nitrosylation of NMDA receptors inhibits Ca2+ influx, conferring neuroprotection.
  • Cellular redox state critically determines NO's neurotoxic or neuroprotective effects.

Conclusions:

  • Protein S-nitrosylation is a crucial regulator of cell function and signal transduction.
  • Modulating NMDA receptor activity via S-nitrosylation presents a therapeutic avenue for neurological conditions.
  • Understanding the redox-dependent actions of NO is vital for developing targeted treatments.

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