Mechanism by which peripheral galanin increases acute inflammatory pain

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 eluc...

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Bibliographic Details
Published in:Brain research 2005-09, Vol.1056 (2), p.113-117
Main Authors: Jimenez-Andrade, Juan Miguel, Zhou, Shengtai, Yamani, Ammar, de Ita, Sandra Valencia, Castañeda-Hernandez, Gilberto, Carlton, Susan M.
Format: Article
Language:English
Subjects:
Animals
Biological and medical sciences
Capsaicin
Dose-Response Relationship, Drug
Drug Interactions
Enzyme Inhibitors - pharmacology
Functional Laterality
Fundamental and applied biological sciences. Psychology
Galanin - administration & dosage
Inflammation - etiology
Male
Naphthalenes - pharmacology
Pain - chemically induced
Pain - complications
Pain Measurement - methods
Peripheral sensitization
Phorbol 12,13-Dibutyrate - pharmacology
PKC
Protein Kinase C - metabolism
Rats
Rats, Wistar
Somesthesis and somesthetic pathways (proprioception, exteroception, nociception)
interoception
electrolocation. Sensory receptors
Time Factors
Vertebrates: nervous system and sense organs
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Summary: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.
ISSN:0006-8993
1872-6240
DOI:10.1016/j.brainres.2005.07.007