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

    21 Scopus citations


    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
    Issue number2
    StatePublished - Sep 21 2005


    • Capsaicin
    • PKC
    • Peripheral sensitization

    ASJC Scopus subject areas

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


    Dive into the research topics of 'Mechanism by which peripheral galanin increases acute inflammatory pain'. Together they form a unique fingerprint.

    Cite this