Relationship between neuronal nitric oxide synthase and NADPH-diaphorase in the dorsal root ganglia during neuropathic pain.
10.4097/kjae.2009.57.3.342
- Author:
Hyun Sook CHO
1
;
Yong Sup SHIN
;
Young Ho LEE
;
Wan Ho CHO
;
Young Kwon KO
Author Information
1. Department of Anesthesia and Pain Medicine, The Catholic University of Korea, Daejeon St. Mary's Hospital, Daejeon, Korea.
- Publication Type:Original Article
- Keywords:
Dorsal root ganglion;
NADPH-diaphorase;
Neuropathic pain;
Nitric oxide synthase
- MeSH:
Animals;
Diagnosis-Related Groups;
Ganglia, Spinal;
Hyperalgesia;
Immunohistochemistry;
Mice;
Mice, Knockout;
Neuralgia;
Neurons;
Nitric Oxide;
Nitric Oxide Synthase;
Nitric Oxide Synthase Type I;
Spinal Nerve Roots;
Spinal Nerves
- From:Korean Journal of Anesthesiology
2009;57(3):342-349
- CountryRepublic of Korea
- Language:English
-
Abstract:
BACKGROUND: Changes in nitric oxide (NO) production in the dorsal root ganglia (DRG) may contribute to allodynia after nerve injury. It is known that the histochemistry of NADPH-diaphorase (NADPH-d) is known to be not always coincident with NOS. This study was conducted to investigate the relationship between nNOS and NADPH-d expression in the DRG in a spinal nerve injury model of neuropathic pain, and to elucidate role that NO plays in neuropathic pain. METHODS: nNOS immunohistochemistry and/or NADHP-d histochemistry were conducted in the DRG of a spinal nerve transection model of neuropathic pain, and the pain behavior was then measured by a von Frey filament test of the hindpaws of wild type and nNOS knock-out mice. RESULTS: nNOS immunoreactive neurons and NADPH-d stained neurons were not always identical. Additionally NADPH-d increased, but nNOS did not increase significantly in the DRG after spinal nerve transection. Neuropathic pain behavior increased in the hindpaw of nNOS(-/-) mice after spinal nerve transection, but was lower than that of wild type mice after spinal nerve transection. CONCLUSIONS: nNOS immunoreactive neurons and NADPH-d stained neurons were not always identical in the DRG, and a novel NADPH-d positive source may be involved in neuropathic pain after spinal nerve transection. Changes in nNOS expression in the DRG were not the primary cause of neuropathic pain behavior in a spinal nerve transection model of neuropathic pain.
