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Related Experiment Videos

Neuronal protection and destruction by NO.

S A Lipton1

  • 1The CNS Research Institute, Brigham and Women's Hospital, and Program in Neuroscience, Harvard Medical School, Boston, MA 02115 USA. Slipton@burnham-inst.org

Cell Death and Differentiation
|November 11, 1999
PubMed
Summary

Different nitric oxide (NO) species offer neuroprotection by modulating neuronal pathways. S-nitrosylation of proteins like NMDARs and caspases, and nitroxyl anion (NO-) interaction with thiols, protect neurons from insults.

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Area of Science:

  • Neuroscience
  • Biochemistry
  • Toxicology

Background:

  • Nitric oxide (NO) and its related species exist endogenously in biological tissues, including the brain.
  • These species have distinct chemical reactivities that influence neuronal survival and death under various insults.
  • S-nitrosylation, a key reaction involving NO+ equivalents, modifies protein function by targeting cysteine residues.

Purpose of the Study:

  • To investigate the neuroprotective mechanisms of different nitric oxide (NO)-related species.
  • To explore the role of S-nitrosylation in regulating neuronal signaling pathways and protein activity.
  • To examine the potential of NO-related species in preventing neuronal damage from insults like excitotoxicity and ischemia/reperfusion.

Main Methods:

  • Physiological and chemical evidence were gathered to support the proposed mechanisms.

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  • Studies focused on the effects of S-nitrosylation on N-methyl-D-aspartate receptor (NMDAR) and caspase activity.
  • The reactions of NO+, NO*, and nitroxyl anion (NO-) with biological molecules, particularly thiols, were investigated.

    • Main Results:

    • S-nitrosylation was shown to decrease NMDAR and caspase activity, offering neuroprotection by inhibiting apoptotic pathways.
    • Nitroglycerin administration was found to be neuroprotective in ischemia/reperfusion models, independent of increased cerebral blood flow.
    • Nitroxyl anion (NO-) was observed to react with NMDA receptor thiols, reducing excessive Ca2+ influx and protecting against excitotoxicity.

    Conclusions:

    • S-nitrosylation acts as a regulatory mechanism, akin to phosphorylation, controlling protein function and providing neuroprotection.
    • Nitroglycerin's neuroprotective effects extend beyond its vasodilatory actions, involving modulation of neuronal pathways.
    • Different redox states of NO play crucial, distinct roles in neuronal function and protection, with NO+ equivalents and NO- offering protective benefits while NO* can be toxic.