Mechanism by which peripheral galanin increases acute inflammatory pain
In: Brain research, Jg. 1056 (2005-03-10), Heft 2
Online
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Zugriff:
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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Mechanism by which peripheral galanin increases acute inflammatory pain
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Autor/in / Beteiligte Person: | Sandra Valencia de Ita ; Juan Miguel Jimenez-Andrade ; Yamani, Ammar ; Castañeda-Hernández, Gilberto ; Zhou, Shengtai ; Carlton, Susan M. |
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Zeitschrift: | Brain research, Jg. 1056 (2005-03-10), Heft 2 |
Veröffentlichung: | 2005 |
Medientyp: | unknown |
ISSN: | 0006-8993 (print) |
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