ID 289
Title Transcription
カプサイシン ト TRP チャネル サブファミリー オヨビ カプサイシン ジュヨウタイ TRPV1 ト コガタ イチジ チカク ニューロン ノ トクセイ ト ソノ ソウカン カンケイ
Title Alternative
Capsaicin, Transient Receptor Potential (TRP) Protein Subfamilies and the Particular Relationship between Capsaicin Receptors and Small Primary Sensory Neurons
Author
Nakagawa, Hiroshi Center for Advanced Dental Health Care, Tokushima University Hospital Tokushima University Educator and Researcher Directory KAKEN Search Researchers
Hiura, Akio Department of Histology and Oral Histology, Institute of Health Biosciences, The University ofTokushima Graduate School KAKEN Search Researchers
Keywords
TRPチャネル
カプサイシン受容体(TRPV1)
侵害受容性ニューロン
一次知覚ニューロン
IB4
Content Type
Departmental Bulletin Paper
Description
A number of subfamilies of the capsaicin receptor, collectively called TRP, have been reported since the discovery of vanilloid receptor 1 (VR1). The term TRP is derived from transient receptor potential, which means the transient and rapid defect of reaction following long stimulation with light in the photoreceptor cells of mutant Drosophila. The common features of TRP family members are the centrally situated six transmembrane domains, in which an ion channel is located. The TRP family members are present in animals, including invertebrates and vertebrates, and in the cells in various tissues in individual animals. During evolution, the original TRP seems to have acquired a wide variety of functions related to sensing the inner or outer environment (e.g. to sensing light: Drosophila), osmolarity, protons, temperature, ligands and mechanical force). In mammals, the TRP subfamily is exclusively expressed in small- to medium-sized primary sensory neurons that also co-express some chemical markers (i.e. isolectin B4: IB4), fluoride-resistant acid phosphatase (FRAP), the P2X_3 purinoceptor (a receptor provoked by ATP-induced nociception) and Ret, a glial cell-line derived neurotrophic factor receptor). There is a paradox in that regardless of the marked or complete loss of noxious, small sensory neurons (polymodal nociceptors) in mice treated with capsaicin during the neonatal period, as well as in VR1 (TRPV1)-deficient knock-out mice, the responses to noxious heat are normal. Regarding the paradox in mice treated with capsaicin as neonates, our explanation is that although capsaicin probably reduces the number of a subgroup of small neurons (IB4-, VR1+), the remaining IB4+ (VR1-) neurons can sense noxious heat normally. One working hypothesis is that mice lacking TRPV1/2 can sense noxious heat under normal conditions, presumably via another still unknown pathway, and TRPV1 has been suggested to be involved in noxious heat transduction under pathological conditions, such as inflammation and tissue injury. Further studies will be required to clarify these complexities. Mice treated with capsaicin as neonates would provide a model to investigate the above paradoxes, as would TRPV1-knock-out mice, although different mechanisms may be operating in the two models. This article is reproduced from the current review published in the Anatomical Science International (Vol. 81, 2006) under the approvals by the chief editor of ASI and Blackwell Publishing.
Journal Title
四国歯学会雑誌
ISSN
09146091
NCID
AN10050046
Volume
19
Issue
2
Start Page
197
End Page
218
Sort Key
197
Published Date
2007-01
Remark
公開日:2010年1月24日で登録したコンテンツは、国立情報学研究所において電子化したものです。
EDB ID
FullText File
language
jpn
departments
University Hospital
Oral Sciences
Report Type
総説