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Nitric oxide and opioid tolerance

A M Babey1, Y Kolesnikov, J Cheng

  • 1Cotzias Laboratory of Neuro-Oncology, Memorial Sloan-Kettering Cancer Center, New York, NY 10021.

Neuropharmacology
|November 1, 1994
PubMed
Summary
This summary is machine-generated.

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Nitric oxide synthase (NOS) inhibition prevents morphine tolerance. Chronic L-arginine administration induces tolerance in opioid-naive mice by activating NOS, highlighting NO's role in opioid analgesia.

Area of Science:

  • Neuroscience
  • Pharmacology

Background:

  • Morphine tolerance is a significant clinical challenge.
  • The role of nitric oxide (NO) in opioid analgesia is not fully understood.

Purpose of the Study:

  • To investigate the role of nitric oxide synthase (NOS) and its substrate L-arginine in the development of morphine tolerance.
  • To explore the potential of modulating NOS activity for pain management.

Main Methods:

  • Administered NG-nitro-L-arginine (NOArg), a NOS inhibitor, and L-arginine to mice.
  • Assessed changes in NOS activity and mRNA levels.
  • Evaluated morphine's analgesic potency using dose-response curves.

Main Results:

  • NOArg treatment prevented morphine tolerance and progressively inhibited NOS activity.

Related Experiment Videos

  • Chronic morphine administration did not alter NOS levels or activity.
  • L-arginine administration alone accelerated morphine tolerance and decreased morphine potency.
  • Chronic L-arginine induced tolerance in opioid-naive mice via NOS.

    • Conclusions:

    • Nitric oxide plays a crucial role in modulating opioid analgesia.
    • Targeting NOS activity presents a potential strategy for managing opioid tolerance.