Involvement of nitric oxide in spinally mediated hyperalgesia in the mouse

Kelley F. Kitto; Jane E. Haley; George L. Wilcox

doi:10.1016/0304-3940(92)90790-E

Involvement of nitric oxide in spinally mediated hyperalgesia in the mouse

Kelley F. Kitto, Jane E. Haley, George L. Wilcox

Neuroscience

Research output: Contribution to journal › Article › peer-review

307 Scopus citations

Abstract

Intrathecal injection of N-methyl-d-aspartate (NMDA) induces a short duration hyperalgesia in mice. An inhibitor of nitric oxide synthase (NOS), N^ω-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 language	English (US)
Pages (from-to)	1-5
Number of pages	5
Journal	Neuroscience Letters
Volume	148
Issue number	1-2
DOIs	https://doi.org/10.1016/0304-3940(92)90790-E
State	Published - 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.

Keywords

Hyperalgesia
NMDA
Nitric oxide
Nociception
Sodium nitroprusside
Synaptic plasticity

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10.1016/0304-3940(92)90790-E

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title = "Involvement of nitric oxide in spinally mediated hyperalgesia in the mouse",

abstract = "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.",

keywords = "Hyperalgesia, NMDA, Nitric oxide, Nociception, Sodium nitroprusside, Synaptic plasticity",

author = "Kitto, {Kelley F.} and Haley, {Jane E.} and Wilcox, {George L.}",

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.",

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AU - Kitto, Kelley F.

AU - Haley, Jane E.

AU - Wilcox, George L.

N1 - 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.

PY - 1992/12/14

Y1 - 1992/12/14

N2 - 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.

AB - 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.

KW - Hyperalgesia

KW - NMDA

KW - Nitric oxide

KW - Nociception

KW - Sodium nitroprusside

KW - Synaptic plasticity

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ER -

Involvement of nitric oxide in spinally mediated hyperalgesia in the mouse

Abstract

Bibliographical note

Keywords

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