Phosphorylation of TRPV1 by neurokinin-1 receptor agonist exaggerates the capsaicin-mediated substance P release from cultured rat dorsal root ganglion neurons
Use this link to cite this item : https://ir.lib.hiroshima-u.ac.jp/00025915
ID | 25915 |
file | |
creator |
Tang, He-Bin
Li, Yu-Sang
Miyano, Kanako
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subject | Dorsal root ganglion neuron
Neurokinin-1 receptor
Phosphorylation of transient receptor potential vanilloid receptor subtype 1
Substance P release
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NDC |
Medical sciences
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abstract | The present study was conducted to determine whether the activation of neurokinin-1 receptor (NK-1R) by its agonist (GR73632) enhances the capsaicin-evoked substance P (SP) release using a radioimmunoassay. A pre-exposure to GR73632 enhanced the capsaicin-evoked SP release in a time- and dose-dependent manner. The augmentation of capsaicin-evoked SP release by GR73632 was completely inhibited by pharmacological blockade of NK-1R or transient receptor potential vanilloid receptor subtype 1 (TRPV1), and was partially attenuated by the inhibition of either protein kinase C (PKC), cyclooxygenase (COX) or phospholipase C (PLC), p38 or p42/44 mitogen-activated protein (MAP) kinase, but not protein kinase A. This augmentation of SP release was further increased by inhibition of c-Jun NH2-terminal kinase. A short-term (10 min) exposure to GR73632 resulted in an increase in the TRPV1 phosphorylation. The increase in the TRPV1 phosphorylated forms induced by a 60-min exposure to GR73632 was completely abolished by the inhibition of either PKC, COX or PLC, p38 or p42/44 MAP kinases. Immunocytochemistry study demonstrated that the NK-1R and TRPV1 were mainly co-expressed in the small-sized neurons. These findings suggest that the activation of NK-1R by its agonist, by sensitizing the TRPV1 through the PKC phosphorylation of TRPV1, may play a role in the enhancement of the capsaicin-evoked SP release from cultured rat DRG neurons.
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journal title |
Neuropharmacology
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volume | Volume 55
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issue | Issue 8
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start page | 1405
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end page | 1411
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date of issued | 2008-12
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publisher | Pergamon-Elsevier Science Ltd.
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issn | 0028-3908
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ncid | |
publisher doi | |
language |
eng
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nii type |
Journal Article
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HU type |
Journal Articles
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DCMI type | text
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format | application/pdf
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text version | author
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rights | Copyright (c) 2009 Elsevier B.V.
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relation url | |
department |
Graduate School of Biomedical Science
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