AIM: To explain the variability in the behavioral response after spinal nerve ligation by investigating the relation between the development of neuropathic pain and the expression of inflammatory indicators, in dorsal root ganglia (DRG) and the spinal nerve. METHODS: Ninety-six male Sprague-Dawley rats were randomly assigned to the modified spinal nerve ligation, sham, and control group. Testing for pain-related behavior identified rats that successfully developed neuropathic pain (responders) and those which did not (non-responders). The extent of neuroinflammation in the two groups was assessed by immunohistochemical staining of dorsal root ganglions glial fibrillary acid protein (GFAP), and rat C3 complement receptor (OX-42). RESULTS: GFAP and OX-42 immunopositive cell density in the DRG and spinal nerve was significantly higher in hyperalgesic animals. DRG cell density was 3.96+/-0.68 cells/2500 microm2 in GFAP responders' group, compared with 2.76+/-0.75 cells/2500 microm2 in non-responders' group (Mann-whitney U test, Z=-3.956, P<0.001). OX-42 density was 7.71+/-1.03 cells/2500 microm2 in responders and 4.75+/-1.76 cells/2500 microm2 in non responders (Mann-whitney U test, Z=-2.572, P=0.01). Hyperalgesic behavior progressively increased during the testing period, although immunopositive cell density peaked on the fourth day post-injury and progressively decreased afterwards. CONCLUSION: Our study suggests that inflammation has a decisive role in initiating neuropathic pain. Also, this study confirms that, for the sake of selecting appropriate subjects for mechanistic study, it is necessary to discriminate between experimental subjects that develop pain completely and those that do not.
AIM: To explain the variability in the behavioral response after spinal nerve ligation by investigating the relation between the development of neuropathic pain and the expression of inflammatory indicators, in dorsal root ganglia (DRG) and the spinal nerve. METHODS: Ninety-six male Sprague-Dawley rats were randomly assigned to the modified spinal nerve ligation, sham, and control group. Testing for pain-related behavior identified rats that successfully developed neuropathic pain (responders) and those which did not (non-responders). The extent of neuroinflammation in the two groups was assessed by immunohistochemical staining of dorsal root ganglions glial fibrillary acid protein (GFAP), and rat C3 complement receptor (OX-42). RESULTS:GFAP and OX-42 immunopositive cell density in the DRG and spinal nerve was significantly higher in hyperalgesic animals. DRG cell density was 3.96+/-0.68 cells/2500 microm2 in GFAP responders' group, compared with 2.76+/-0.75 cells/2500 microm2 in non-responders' group (Mann-whitney U test, Z=-3.956, P<0.001). OX-42 density was 7.71+/-1.03 cells/2500 microm2 in responders and 4.75+/-1.76 cells/2500 microm2 in non responders (Mann-whitney U test, Z=-2.572, P=0.01). Hyperalgesic behavior progressively increased during the testing period, although immunopositive cell density peaked on the fourth day post-injury and progressively decreased afterwards. CONCLUSION: Our study suggests that inflammation has a decisive role in initiating neuropathic pain. Also, this study confirms that, for the sake of selecting appropriate subjects for mechanistic study, it is necessary to discriminate between experimental subjects that develop pain completely and those that do not.
Authors: Samantha Dayawansa; Ernest W Wang; Weimin Liu; John D Markman; Harris A Gelbard; Jason H Huang Journal: Neurol Res Date: 2014-05-18 Impact factor: 2.448
Authors: Jennifer A Stokes; Jonathan Cheung; Kelly Eddinger; Maripat Corr; Tony L Yaksh Journal: J Neuroinflammation Date: 2013-12-09 Impact factor: 8.322