Neurotrophin-3 and tyrosine kinase C have modulatory effects on neuropathic pain in the rat dorsal root ganglia

Gabriel C Tender, Alan David Kaye, Yuan-Yuan Li, Jian-Guo Cui
Neurosurgery 2011, 68 (4): 1048-55; discussion 1055

BACKGROUND: Neurotrophin-3 (NT3) and its cognate receptor, tyrosine kinase C (TrkC), have recently been shown to modulate neuropathic pain. Another receptor, the transient receptor potential vanilloid 1, is considered a molecular integrator for nociception. Transient receptor potential vanilloid 1-positive cells can be selectively ablated by Resiniferatoxin (RTX). NT3 changes in the dorsal root ganglia (DRG) after RTX treatment may further define their role in pain modulation.

OBJECTIVE: To demonstrate the role of NT3 and TrkC in intraganglial RTX-induced pain suppression and in neuropathic pain development.

METHODS: Fifty-three rats underwent a photochemical left sciatic nerve injury. Neuropathic animals were treated by RTX injection in the ipsilateral L3-6 DRG. NT3 and TrkC presence in the DRG was evaluated before and after the nerve injury, as well as after RTX treatment.

RESULTS: The RTX injection resulted in pain inhibition. NT3 normally expressed mainly in large- and medium-size neurons. NT3 presence was increased mainly in the small DRG cells of neuropathic animals, and the medium- and large-size neurons of nonallodynic rats. RTX treatment of allodynic rats changed the NT3 distribution to a nonallodynic pattern. TrkC expressed mainly in large/medium-size neurons. After nerve injury, TrkC expression was also increased in the small DRG cells of allodynic animals (although less than NT3), and the medium- and large-size cells of nonallodynic ones. After RTX, TrkC expression gradually decreased, but with persistence in the large DRG cells.

CONCLUSION: NT3 may have antinociceptive effects in the DRG. These effects may be mediated, at least in part, by TrkC in the medium- and large-size DRG neurons.

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