Effect of Nitric Oxide on Neuropeptide Y Immunoreactivity in Rat Spinal Cord on the Allodynia of Inflammation Induced by Freund's Complete Adjuvant.
- Author:
Seung Jun HWANG
1
;
Da Young SHIN
;
Tai Jin CHUNG
;
Min Hee KIM
;
Hae Nam HONG
;
Yoon CHOI
Author Information
1. Department of Anatomy and Cell Biology, University of Ulsan, College of Medicine, Seoul, Korea. sjhwang@amc.seoul.kr
- Publication Type:Original Article
- Keywords:
FCA;
Allodynia;
Spinal cord;
NO;
L-NAME;
NPY
- MeSH:
Animals;
Arginine;
Horns;
Hyperalgesia*;
Inflammation*;
Injections, Subcutaneous;
Neurons;
Neuropeptide Y*;
Neuropeptides*;
NG-Nitroarginine Methyl Ester;
Nitric Oxide*;
Rats*;
Spinal Cord*
- From:Korean Journal of Anatomy
2001;34(6):579-588
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
Injection of Freund's complete adjuvant (FCA) into peripheral tissue induces inflammatory responses with accompanying pain behaviors. Injection of FCA produced a significant mechanical allodynia over time and nitric oxide(NO) is involved in this mechanism. The role of neuropeptide Y (NPY) on allodynia induced by inflammation is still controversal. We invastigated the change of spinal NPY and nitric oxide in rats with inflammation induced by subcutaneous injection of FCA and L-NG-nitro arginine methyl ester (L-NAME) into hind paw. The results are: The number of NADPH-diaphorase positive neurons and staining intensity of area increased at ipsilateral spinal ventral/dorsal horn of inflammation model. No significant changes were found with L-NAME posttreatment. Staining intensity of NPY immunoreactive (ir) area increased at ipsilateral spinal dorsal horn after FCA injection. No significant changes were found with L-NAME posttreatment. NPY-ir and NADPH-d reactive neurons were found in Rexed III-IV lamina at spinal dorsal horn. No significant change were found on all groups. The results suggest that spinal NPY is involved in the mechanism of the development and maintenance of allodynia in a state of FCA-induced inflammaion. NO may be also involved in the regulation of the quantity of NPY in spinal cord level.
