Effect of Nitric Oxide on the Change of Spinal Neuropeptide in the Inflammation Model by Freund's Complete Adjuvant / 대한해부학회지

Injection of Freund's complete adjuvant (FCA) into the plantar surface of the rat induces inflammatory responses with accompanying pain behaviors. Signs of pain behaviors observed in FCA-injected animals are reported to be similar to symptoms seen in patients with inflammatory pain. In the previous study, injection of FCA produced a significant mechanical allodynia over time. The role of substance-P and calcitonin gene-related peptide(CGRP) on allodynia induced by inflammation is still controversial. We investigated the change of spinal neuropeptides and nitric oxide (NO) in rats with inflammation induced by subcutaneous injection of FCA into hind paw. The results are: 1. The number of NADPH-diaphorase and substance P positive neurons increased at ipsilateral spinal ventral horn after FCA injection. No significant changes were found with L-NAME posttreatment. 2. Staining intensity of substance P-immunoreactive area increased at ipsilateral spinal dorsal horn after FCA injection. No significant changes were found with L-NAME posttreatment. 3. CGRP immunoreactivity changed in the same pattern with substance P in all group. The results suggest that spinal neuropeptide substance P and CGRP are 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 substance P and CGRP in spinal cord.

Effect of Nitric Oxide on Neuropeptide Y Immunoreactivity in Rat Spinal Cord on the Allodynia of Inflammation Induced by Freund's Complete Adjuvant / 대한해부학회지

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.

A change of nitric oxide in rat DRG following Freund's Complete Adjuvant induced inflammtory pain / 대한해부학회지

It has been reported that injection of Freund's complete adjuvant (FCA) into the hindpaw of a rat induces inflammatory responses with accompanying pain behaviors. Signs of pain behaviors observed in FCA-injected animals were reported to be similar to symptoms seen in patients with inflammatory pain. The nicotinamide adenine dinucleotide phosphate-diaphorase (NADPH-d) is a selective histochemical marker for the nitric oxide synthesizing enzyme, nitric oxide synthase (NOS). N (G)-nitro-L-arginine methyl ester (L-NAME) is a NOS inhibitor. In the present study, we examined if inflammaory pain causes increases in NADPH-diaphorase reactivities in neurons of the dorsal root ganglia (DRG). The results were as follows; 1. FCA-induced inflammation on a limb increased staining density (SD) of NADPH-d positive neurons in the ipsilateral side DRG. 2. Pretreatment of L-NAME did not changed SD of NADPH-d positive neurons on the inflammation of contralateral side DRG 3. Posttreatment of L-NAME decreased the inflammation induced SD of NADPH-d positive neurons. 4. n-NOS immunoreactivity did not match NADPH-d histochemical study, implying the constant level of enzyme itself. Inflammation pain on a hindlimb increased staining density of NADPH-diaphorase positive neuron in the DRG, which was decreased by L-NAME. L-NAME also decreased pain perception. This suggests a role of NO in the pain perception and/or modulation at the level of DRG.