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Oral Sensory mechanism of Capsaicin and thermal stimulation

Research Project

Project/Area Number 17591916
Research Category

Grant-in-Aid for Scientific Research (C)

Allocation TypeSingle-year Grants
Section一般
Research Field Morphological basic dentistry
Research InstitutionKYUSHU UNIVERCITY

Principal Investigator

KIDO Mizuho  Kyushu University, Faculty of Dental Science, Associate Professor, 大学院歯学研究院, 助教授 (60253457)

Co-Investigator(Kenkyū-buntansha) ZHANG Jing-Qi  Kyushu University, Faculty of Dental Science, Research Assistant, 大学院歯学研究院, 技術専門職員 (80380707)
TANAKA Teruo  Kyushu University, Faculty of Dental Science, Professor, 大学院歯学研究院, 教授 (60077667)
Project Period (FY) 2005 – 2006
Project Status Completed (Fiscal Year 2006)
Budget Amount *help
¥3,500,000 (Direct Cost: ¥3,500,000)
Fiscal Year 2006: ¥1,000,000 (Direct Cost: ¥1,000,000)
Fiscal Year 2005: ¥2,500,000 (Direct Cost: ¥2,500,000)
Keywordscapsaicin / taste / hot / pain / rat / tongue
Research Abstract

The ingestion of spicy food containing hot chili peppers evokes an oral tingling and burning sensation. Much interest in pain perception has recently focused on capsaicin, the pungent ingredient in hot pepper, and its molecular target, vanilloid receptor 1 (TRPV1, VR1), which is a nociceptive-specific cation channel. We demonstrated that the taste papillae of the tongue and palate are richly innervated with TRPV1 immunoreactive nerves. It is well known that extracellular signal-regulated kinase (ERK) is a mitogen activated protein kinase (MAPK) that mediates several cellular responses to mitogenic and differentiation signals. MAPK are activated not only during growth factor signaling but in neuronal plasticity as well. Very recently it is reported that phosphorylation of ERK in primary afferent neurons occurred in response to noxious stimulation of the peripheral nerve. Then, to elucidate the sensory mechanisms of oral sensation, including hot taste, we examined the rapid phosphorylation of ERK (pERK) in primary afferent nerves in the oral mucosa after stimulation with capsaicin to the oral cavity. After intraoral capsaicin stimulation, the amount of pERK labeling was clearly increased compared with the vehicle treated rats. Interestingly, abundant labeled fibers were observed in the taste buds of circumvallate and foliate papillae. The pERK-labeled nerves were also labeled with P2X3 or CGRP. Some of the nerves were labeled with IB4 lectin. Capsaicin stimulation caused rapid phosphorylation of ERK in the peripheral nerves of the oral mucosa, suggesting that these nerves are of great importance in the perception of capsaicin and that ERK activation is involved in oral sensitization.

Report

(3 results)
  • 2006 Annual Research Report   Final Research Report Summary
  • 2005 Annual Research Report

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Published: 2005-04-01   Modified: 2016-04-21  

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