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Korean J Anesthesiol > Volume 57(3); 2009 > Article
Korean Journal of Anesthesiology 2009;57(3):342-349.
DOI: https://doi.org/10.4097/kjae.2009.57.3.342   
Relationship between neuronal nitric oxide synthase and NADPH-diaphorase in the dorsal root ganglia during neuropathic pain.
Hyun Sook Cho, Yong Sup Shin, Young Ho Lee, Wan Ho Cho, Young Kwon Ko
1Department of Anesthesia and Pain Medicine, The Catholic University of Korea, Daejeon St. Mary's Hospital, Daejeon, Korea.
2Department of Anesthesiology and Pain Medicine, Chungnam National University, School of Medicine, Daejeon, Korea. ysshin@cnu.ac.kr
3Department of Anatomy, Chungnam National University, School of Medicine, Daejeon, Korea.
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.
Key Words: Dorsal root ganglion; NADPH-diaphorase; Neuropathic pain; Nitric oxide synthase
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