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
Painjournal_title
Painauthors
Sun YG,Gracias NG,Drobish JK,Vasko MR,Gereau RW,Chen ZFdoi
10.1016/j.pain.2009.04.011subject
Has Abstractpub_date
2009-07-01 00:00:00pages
178-86issue
1-2eissn
0304-3959issn
1872-6623pii
S0304-3959(09)00217-6journal_volume
144pub_type
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