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ID 289
タイトルヨミ
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
タイトル別表記
Capsaicin, Transient Receptor Potential (TRP) Protein Subfamilies and the Particular Relationship between Capsaicin Receptors and Small Primary Sensory Neurons
著者
中川, 弘 徳島大学医学部・歯学部附属病院高次歯科診療部 徳島大学 教育研究者総覧 KAKEN研究者をさがす
樋浦, 明夫 徳島大学大学院ヘルスバイオサイエンス研究部口腔組織学分野 KAKEN研究者をさがす
キーワード
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
資料タイプ
紀要論文
抄録
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.
掲載誌名
四国歯学会雑誌
ISSN
09146091
cat書誌ID
AN10050046
19
2
開始ページ
197
終了ページ
218
並び順
197
発行日
2007-01
備考
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
フルテキストファイル
言語
jpn
部局
病院
歯学系
記事種別
総説