CHANGES IN CD200 AND CD200R EXPRESSION IN TWO RAT MODELS OF NEUROPATHIC PAIN

Investor logo
Investor logo
Investor logo

Warning

This publication doesn't include Faculty of Medicine. It includes Central European Institute of Technology. Official publication website can be found on muni.cz.
Authors

HERNANGÓMEZ HERRERO Miriam DUBOVÝ Petr HRADILOVÁ SVÍŽENSKÁ Ivana KLUSÁKOVÁ Ilona

Year of publication 2013
Type Appeared in Conference without Proceedings
MU Faculty or unit

Central European Institute of Technology

Citation
Description Background and aim. The existence of CD200 in glial cells and neurons of the central nervous system is well-known, but there is limited information on the distribution of CD200 and CD200R in the peripheral nervous system. Here, we investigate bilateral changes of CD200 and CD200R expression in L4-L5 dorsal root ganglia (DRG) after chronic constriction (CCI) or spare nerve (SNI) injury of the sciatic nerve used as neuropathic pain models. Method. Rats undergoing unilateral CCI and SNI were left to survive for 3, 7 or 14 days, sham-operated rats for 3 or 14 days. Neuropathic pain induction was tested by measurement of mechanoallodynia and thermal hyperalgesia. After the survival time, L4-L5 DRG were removed bilaterally from naive, operated, and sham-operated rats and CD200 and CD200R proteins were detected by immunohistochemical staining. Results. Unilateral SNI induced a transient bilateral increase of CD200 protein levels in satellite glial cells after 3 days while immunostaining was reduced following 14 days from operation. In contrast, CD200 immunofluorescence was elevated bilaterally in DRG mainly after 14 days from CCI operation. Furthermore, CD200R expression was enhanced in DRG after 7 days from SNI and CCI operations compared with naive animals. Conclusion. Our results suggest that CD200/CD200R might play an inhibitory role of neuroinflammatory reactions in the DRG to keep homeostasis after neuropathic stress.
Related projects:

You are running an old browser version. We recommend updating your browser to its latest version.

More info