| First Author | Sun YG | Year | 2009 |
| Journal | Pain | Volume | 144 |
| Issue | 1-2 | Pages | 178-86 |
| PubMed ID | 19443120 | Mgi Jnum | J:157362 |
| Mgi Id | MGI:4430701 | Doi | 10.1016/j.pain.2009.04.011 |
| Citation | Sun YG, et al. (2009) The c-kit signaling pathway is involved in the development of persistent pain. Pain 144(1-2):178-86 |
| abstractText | 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. |
