| Article ID | Journal | Published Year | Pages | File Type |
|---|---|---|---|---|
| 9416011 | Brain Research | 2005 | 5 Pages |
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 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.
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Authors
Juan Miguel Jimenez-Andrade, Shengtai Zhou, Ammar Yamani, Sandra Valencia de Ita, Gilberto Castañeda-Hernandez, Susan M. Carlton,