TY - JOUR
T1 - Mechanism by which peripheral galanin increases acute inflammatory pain
AU - Jimenez-Andrade, Juan Miguel
AU - Zhou, Shengtai
AU - Yamani, Ammar
AU - Valencia De Ita, Sandra
AU - Castañeda-Hernandez, Gilberto
AU - Carlton, Susan M.
N1 - Funding Information:
The authors would like to thank Vicki Wilson for her excellent secretarial assistance. This work was supported by NIH NS40700 and NS27910 to SMC and by CONACyT grant 38940-M to GCH. JMJA is a CONACyT fellow from Mexico.
PY - 2005/9/21
Y1 - 2005/9/21
N2 - 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.
AB - 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.
KW - Capsaicin
KW - PKC
KW - Peripheral sensitization
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U2 - 10.1016/j.brainres.2005.07.007
DO - 10.1016/j.brainres.2005.07.007
M3 - Article
C2 - 16125151
AN - SCOPUS:27644495854
SN - 0006-8993
VL - 1056
SP - 113
EP - 117
JO - Brain Research
JF - Brain Research
IS - 2
ER -