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
Capsaicin, Transient Receptor Potential (TRP) Protein Subfamilies and the Particular Relationship between Capsaicin Receptors and Small Primary Sensory Neurons
Nakagawa, Hiroshi Center for Advanced Dental Health Care, Tokushima University Hospital Tokushima University Educator and Researcher Directory KAKEN Search Researchers
Departmental Bulletin Paper
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.
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