Involvement of nitric oxide in spinally mediated hyperalgesia in the mouse

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Intrathecal injection of N-methyl-d-aspartate (NMDA) induces a short duration hyperalgesia in mice. An inhibitor of nitric oxide synthase (NOS), Nω-nitro-l-arginine methyl ester (l-NAME), administered either systemically or intrathecally, blocked the NMDA-induced hyperalgesia. This effect was partially reversed by the NOS substrate, l-arginine. Intrathecal hemoglobin mimicked the effects of l-NAME. Intrathecal injection of the NO-donating compounds, sodium nitroprusside (SNP) and hydroxylamine, resulted in a hyperalgesia that lasted 3 h and was reduced by coadministration of hemoglobin. Thus, nitric oxide production appears to mediate NMDA-induced hypersensitivity and may contribute to other forms of centrally induced hyperalgesia.

Original languageEnglish (US)
Pages (from-to)1-5
Number of pages5
JournalNeuroscience Letters
Issue number1-2
StatePublished - Dec 14 1992

Bibliographical note

Funding Information:
The authors wish to thank Dr. Leonard Lichtblau for expert assistance with the data analysis. This work was supported by USPHS Grants R01-DA-04274, R01-DA-01933 and K-02-DA-00145 to G.L.W.


  • Hyperalgesia
  • NMDA
  • Nitric oxide
  • Nociception
  • Sodium nitroprusside
  • Synaptic plasticity


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