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Brain Res. 2005 Sep 21;1056(2):113-7.

Mechanism by which peripheral galanin increases acute inflammatory pain.

Author information

1
Seccion Externa de Farmacologia, Centro de Investigacion y de Estudios Avanzados del Instituto Politecnico Nacional, Mexico, D.F., Mexico.

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.

PMID:
16125151
DOI:
10.1016/j.brainres.2005.07.007
[Indexed for MEDLINE]

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