Mechanism by which peripheral galanin increases acute inflammatory pain

Juan Miguel Jimenez-Andrade; Shengtai Zhou; Ammar Yamani; Sandra Valencia De Ita; Gilberto Castañeda-Hernandez; Susan M. Carlton

doi:10.1016/j.brainres.2005.07.007

Mechanism by which peripheral galanin increases acute inflammatory pain

Juan Miguel Jimenez-Andrade
, Shengtai Zhou
, Ammar Yamani
, Sandra Valencia De Ita
, Gilberto Castañeda-Hernandez
, Susan M. Carlton

Neurobiology

Research output: Contribution to journal › Article › peer-review

24 Scopus citations

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 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.

Original language	English (US)
Pages (from-to)	113-117
Number of pages	5
Journal	Brain Research
Volume	1056
Issue number	2
DOIs	https://doi.org/10.1016/j.brainres.2005.07.007
State	Published - Sep 21 2005

Keywords

Capsaicin
PKC
Peripheral sensitization

ASJC Scopus subject areas

General Neuroscience
Molecular Biology
Clinical Neurology
Developmental Biology

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10.1016/j.brainres.2005.07.007

Cite this

@article{9d2a395af35b4c4292ba922b82c1c145,

title = "Mechanism by which peripheral galanin increases acute inflammatory pain",

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 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.",

keywords = "Capsaicin, PKC, Peripheral sensitization",

author = "Jimenez-Andrade, \{Juan Miguel\} and Shengtai Zhou and Ammar Yamani and \{Valencia De Ita\}, Sandra and Gilberto Casta{\~n}eda-Hernandez and Carlton, \{Susan M.\}",

note = "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.",

year = "2005",

month = sep,

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doi = "10.1016/j.brainres.2005.07.007",

language = "English (US)",

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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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UR - https://www.scopus.com/pages/publications/27644495854#tab=citedBy

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DO - 10.1016/j.brainres.2005.07.007

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AN - SCOPUS:27644495854

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VL - 1056

SP - 113

EP - 117

JO - Brain Research

JF - Brain Research

IS - 2

ER -

Mechanism by which peripheral galanin increases acute inflammatory pain

Abstract

Keywords

ASJC Scopus subject areas

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