Elsevier

Neuroscience Letters

Volume 184, Issue 1, 16 January 1995, Pages 5-8
Neuroscience Letters

Role of peri-axonal inflammation in the development of thermal hyperalgesia and guarding behavior in a rat model of neuropathic pain☆

https://doi.org/10.1016/0304-3940(94)11154-BGet rights and content

Abstract

Loose ligation of a rat's sciatic nerve produces hyperalgesia to thermal stimuli and elicits guarding behavior directed at the afflicted paw. The present experiments test whether localized inflammation induced by the suture material used to ligate the nerve is critical to the development of hyperalgesia. Daily injections of dexamethasone reduced the inflammatory response induced by the sutures and blocked the development of guarding behavior and thermal hyperalgesia. In a second experiment inflammation associated with cotton sutures was enhanced by soaking the sutures in Freund's adjuvant prior to ligation. This caused an augmentation of thermal hyperalgesia and guarding behavior. These results suggest that inflammation around the nerve is critical for the development of guarding behavior and thermal hyperalgesia in this model of neuropathic pain.

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    Interestingly, in CCI females the onset of mechanical allodynia development was asynchronous between experimental groups, with gonadally intact females displaying mechanical allodynia two weeks after ovariectomized females, with increasingly lower withdrawal thresholds throughout the experimental weeks, unlike their ovariectomized counterparts. Altogether, these results point to a role of gonadal hormones on both the early development and maintenance of CCI-induced allodynia, as oestrogen has been reported to enhance the severity of inflammatory responses (Da Silva et al., 1993), crucial for the development of neuropathic pain after ligation of the sciatic nerve (Clatworthy et al., 1995). Also, it was shown ovariectomy can regulate the levels of Fos protein in the spinal dorsal horn, which can, in turn, regulate pain sensitivity (Zhao et al., 2005).

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This research was supported by National Science Foundation Grant IBN-9210268 to E.T.W., a Program Project Grant POI-DK-37260, NIDDKD, NIH to G.A.C, and the Initiative in Mucosal Biology, President's Office, The University of Texas Houston Health Science Center.

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