Mechanism by which peripheral galanin increases acute inflammatory pain

Juan Miguel Jimenez-Andrade, Shengtai Zhou, Ammar Yamani, Sandra Valencia De Ita, Gilberto Castañeda-Hernandez, Susan M. Carlton

Research output: Contribution to journalArticlepeer-review

23 Scopus citations

Abstract

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 pronociceptive 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.

Original languageEnglish (US)
Pages (from-to)113-117
Number of pages5
JournalBrain Research
Volume1056
Issue number2
DOIs
StatePublished - Sep 21 2005

Keywords

  • Capsaicin
  • PKC
  • Peripheral sensitization

ASJC Scopus subject areas

  • General Neuroscience
  • Molecular Biology
  • Clinical Neurology
  • Developmental Biology

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