The c-kit signaling pathway is involved in the development of persistent pain.

Abstract:

:Protein kinase signal transduction pathways play critical roles in regulating nociception. Here we show that c-kit, a tyrosine kinase receptor, is expressed in lamina I and II layer of the dorsal horn. Moreover, the superficial c-kit(+) fibers originate from the dorsal root ganglion, and c-kit in lamina II inner layer comes from intrinsic expression of the spinal cord. Kit(W-v) mice, which contain a hypomorphic mutation, exhibited normal acute pain in most pain behavior tests. In the formalin test, the first phase was not affected, whereas the second phase pain response of Kit(W-v) mice was significantly reduced relative to wild-type littermates. Kit(W-v) mice also showed abnormal neuropathic pain, notably in the contralateral side of nerve injury. The expression and release of CGRP and substance P were not altered by the c-kit mutation. Together, these results implicate c-kit-mediated signal transduction in the development of persistent pain.

journal_name

Pain

journal_title

Pain

authors

Sun YG,Gracias NG,Drobish JK,Vasko MR,Gereau RW,Chen ZF

doi

10.1016/j.pain.2009.04.011

subject

Has Abstract

pub_date

2009-07-01 00:00:00

pages

178-86

issue

1-2

eissn

0304-3959

issn

1872-6623

pii

S0304-3959(09)00217-6

journal_volume

144

pub_type

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