Contribution of protein kinase C to central sensitization and persistent pain following tissue injury

Neurosci Lett. 1992 Jun 22;140(2):181-4. doi: 10.1016/0304-3940(92)90097-q.


This paper provides evidence that central sensitization and persistent nociception following formalin-induced tissue injury in rats is dependent on the production of protein kinase C. Persistent nociceptive behavior in rats induced by subcutaneous formalin injection was significantly reduced by intrathecal pretreatment with a phospholipase C inhibitor (neomycin), and an inhibitor of protein kinase C (W-7), and was significantly enhanced by a phorbol ester (phorbol 12-myristate 13-acetate, PMA) and a stimulator of protein kinase C (SC-10). It is expected that noxious inputs associated with tissue injury produce a release of aspartate and glutamate within the spinal dorsal horn which by acting at ionotropic (NMDA) and metabotropic excitatory amino acid receptors produce an increase in intracellular messengers such as calcium and diacylglycerol which stimulate protein kinase C.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Calcium / metabolism
  • Hyperalgesia / enzymology*
  • Male
  • Neomycin / pharmacology
  • Pain / enzymology*
  • Pain Measurement
  • Protein Kinase C / metabolism
  • Rats
  • Sulfonamides / pharmacology
  • Tetradecanoylphorbol Acetate / pharmacology


  • Sulfonamides
  • W 7
  • Protein Kinase C
  • Neomycin
  • Tetradecanoylphorbol Acetate
  • Calcium