Intracellular signaling in primary sensory neurons and persistent pain.

Published

Journal Article (Review)

During evolution, living organisms develop a specialized apparatus called nociceptors to sense their environment and avoid hazardous situations. Intense stimulation of high threshold C- and Adelta-fibers of nociceptive primary sensory neurons will elicit pain, which is acute and protective under normal conditions. A further evolution of the early pain system results in the development of nociceptor sensitization under injury or disease conditions, leading to enhanced pain states. This sensitization in the peripheral nervous system is also called peripheral sensitization, as compared to its counterpart, central sensitization. Inflammatory mediators such as proinflammatory cytokines (TNF-alpha, IL-1beta), PGE(2), bradykinin, and NGF increase the sensitivity and excitability of nociceptors by enhancing the activity of pronociceptive receptors and ion channels (e.g., TRPV1 and Na(v)1.8). We will review the evidence demonstrating that activation of multiple intracellular signal pathways such as MAPK pathways in primary sensory neurons results in the induction and maintenance of peripheral sensitization and produces persistent pain. Targeting the critical signaling pathways in the periphery will tackle pain at the source.

Full Text

Duke Authors

Cited Authors

  • Cheng, J-K; Ji, R-R

Published Date

  • October 2008

Published In

Volume / Issue

  • 33 / 10

Start / End Page

  • 1970 - 1978

PubMed ID

  • 18427980

Pubmed Central ID

  • 18427980

Electronic International Standard Serial Number (EISSN)

  • 1573-6903

Digital Object Identifier (DOI)

  • 10.1007/s11064-008-9711-z

Language

  • eng

Conference Location

  • United States