Mechanism by which peripheral galanin increases acute inflammatory pain

Brain Res. 2005 Sep 21;1056(2):113-7. doi: 10.1016/j.brainres.2005.07.007.


Galanin (GAL) is a neuropeptide involved in pain transmission. Intraplantar GAL at low doses enhances capsaicin (CAP)-induced pain behaviors in rat, suggesting an excitatory role for GAL under acute inflammatory conditions. The mechanisms underlying this pro-nociceptive action have not yet been elucidated. Thus, the present study investigated the role of protein kinase C (PKC) in the GAL enhancement of CAP-induced inflammatory pain. Ipsilateral, but not contralateral, calphostin C, a PKC inhibitor, blocked GAL-induced potentiation of CAP-evoked inflammatory pain in a dose-dependent fashion. Peripheral activation of PKC using the phorbol ester phorbol-12-myristate-13-acetate (PMA) mimicked the pro-nociceptive effect of GAL. These results suggest that GAL enhances acute inflammatory pain through activation of PKC intracellular pathways.

Publication types

  • Comparative Study
  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Animals
  • Capsaicin*
  • Dose-Response Relationship, Drug
  • Drug Interactions
  • Enzyme Inhibitors / pharmacology
  • Functional Laterality
  • Galanin / administration & dosage*
  • Inflammation / etiology
  • Male
  • Naphthalenes / pharmacology
  • Pain / chemically induced*
  • Pain / complications
  • Pain Measurement / methods
  • Phorbol 12,13-Dibutyrate / pharmacology
  • Protein Kinase C / metabolism
  • Rats
  • Rats, Wistar
  • Time Factors


  • Enzyme Inhibitors
  • Naphthalenes
  • calphostin complex
  • Phorbol 12,13-Dibutyrate
  • Galanin
  • Protein Kinase C
  • Capsaicin