Pain and inflammation
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TL;DR
Ongoing pain and tenderness (allodynia and hyperalgesia) induced by inflammation have to be distinguished and whether recruitment of afferent nerve fibers which are silent in healthy tissue is an important mechanism of inflammatory pain is an open question.
Abstract
The functional regeneration of C-fibers mediating polymodal nociception and low-threshold mechanoreceptive axons in the lateral plantar nerve (LPN) and the foot branch of the superficial peroneal nerve (fSPN) was evaluated in normal rats and 3 months after unilateral sciatic nerve crush or neurotomy and suture. The area covered by low-threshold mechanoreceptors (LTMs) was tested through gentle mechanical skin stimulation and recording from the relevant nerve. In regenerated animals the glabrous skin area with functional LPN-related LTMs was severely reduced following a crush lesion. Functional receptors of that type were absent after neurotomy and suture. The hairy skin area with fSPN-related LTMs was smaller than normal, particularly following neurotomy and suture. The distribution of polymodal C-fibers was tested through stimulation-induced extravasation of Evans blue albumin (EBA). In the glabrous LPN skin domain the area showing EBA extravasation did not return to normal after any of the lesion types. However, in the hairy fSPN skin area the distribution of EBA extravasation appeared largely normal following both injuries. We conclude that polymodal nociception reappears to a greater extent than low threshold mechanosensitivity, and that both modalities regenerate better in hairy skin than in glabrous skin.
