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

Research output: Contribution to journalArticle

14 Scopus citations


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. KitW-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 KitW-v mice was significantly reduced relative to wild-type littermates. KitW-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.

Original languageEnglish (US)
Pages (from-to)178-186
Number of pages9
Issue number1-2
StatePublished - Jul 1 2009



  • c-kit
  • CCI
  • DRG
  • Formalin test
  • Persistent pain
  • Spinal cord
  • Tyrosine kinase receptor

ASJC Scopus subject areas

  • Clinical Neurology
  • Anesthesiology and Pain Medicine
  • Neurology
  • Pharmacology

Cite this

Sun, Y. G., Gracias, N. G., Drobish, J. K., Vasko, M. R., Gereau, R. W., & Chen, Z. F. (2009). The c-kit signaling pathway is involved in the development of persistent pain. Pain, 144(1-2), 178-186.