Changes of Neuropathic Pain in nNOS Knock-out Mice.
10.11637/kjpa.2005.18.4.303
- Author:
Min Jeong KIM
1
;
Su Sung SONG
;
Woo Kyun MOK
;
Jun Young YANG
;
Keon Su LEE
;
Young Ho LEE
Author Information
1. Department of Anatomy, College of Medicine, Chungnam National University. yhlee@cnu.ac.kr
- Publication Type:Original Article
- Keywords:
nNOS;
Neuropathic pain;
Allodynia;
Nitric oxide
- MeSH:
Acetone;
Animals;
Ganglia, Spinal;
Hyperalgesia;
Ligation;
Mice;
Mice, Knockout*;
Nervous System;
Neuralgia*;
NG-Nitroarginine Methyl Ester;
Nitric Oxide;
Peripheral Nervous System Diseases;
Spinal Cord;
Spinal Nerves
- From:Korean Journal of Physical Anthropology
2005;18(4):303-312
- CountryRepublic of Korea
- Language:English
-
Abstract:
Changes in nitric oxide production in spinal cord or dorsal root ganglion have been known to contribute to allodynia after nerve injury. However, regulation of nNOS expression was also reported not to be responsible for the development and/or maintenance of neuropathic allodynia. The aim of this study was to elucidate role of nNOS expression in the sensory nervous system in neuropathic pain. Von Frey and acetone tests were performed in a model of peripheral neuropathy, ligation of 5th lumbar and 6th lumbar spinal nerves, in wild type and nNOS (-/-) mice. The effect of nNOS inhibitor was evaluated in neuropathic pain behavior in the mice. Mechanical allodynia was slightly reduced in nNOS (-/-) mice compared with wild type mice after peripheral neuropathy. nNOS inhibitor, L-NAME, reduced minimally mechanical allodynia, not cold allodynia, but gabapentin reduced remarkably neuropathic pain behavior (mechanical and cold allodynia) in both wild type and nNOS (-/-) mice. These results suggested that nNOS expression in the sensory nervous system may be partially associated with development and/or maintenance of mechanical allodynia in a mouse model of peripheral neuropathy.
