Okumura Reijiro, Shima Kaori, Muramatsu Takashi, Nakagawa Kan-Ichi, Shimono Masaki, Suzuki Takashi, Magloire Henry, Shibukawa Yoshiyuki
Department of Physiology, Tokyo Dental College, Chiba, Japan.
Arch Histol Cytol. 2005 Dec;68(4):251-7. doi: 10.1679/aohc.68.251.
Previous reports have shown the expression of several mechanosensitive ionic channels on the plasma membrane in odontoblasts, which are the cells responsible for dentin formation. The membrane characteristics of odontoblasts imply that they could play critical roles in the mechano-transduction of fluid displacement within dentinal tubules into the electrical cell signals, to carry dentin sensation to the central nervous system. However, the direct ionic mechanism underlying such a dentin nociceptive function remains unclear. In the present study, we investigated the expression of the transient receptor potential vanilloid subfamily member 1 (TRPV1) channel--which essentially contributes to the detection of pain sensation--in rat odontoblasts by immunohistochemical and nystatin perforated patch-clamp techniques. Immunohistochemical observation showed the localization of TRPV1-immunoreactions on the distal regions of odontoblast membranes. In the patch-clamp experiments, we observed capsaicin-induced inward currents that were inhibited by capsazepine, a TRPV1 channel antagonist. Our results indicate a significant expression of TRPV1 channels in odontoblasts, suggesting that odontoblasts may directly respond to noxious stimuli such as a thermal-heat stimulus, and point to the necessity for a reconsideration of the cellular mechanisms of dentin sensation based on the transmembrane ionic signals in odontoblasts.
先前的报道显示，在成牙本质细胞（负责牙本质形成的细胞）的质膜上存在几种机械敏感离子通道的表达。成牙本质细胞的膜特性表明，它们可能在将牙本质小管内的液体位移机械转导为细胞电信号以将牙本质感觉传递到中枢神经系统的过程中发挥关键作用。然而，这种牙本质伤害感受功能背后的直接离子机制仍不清楚。在本研究中，我们通过免疫组织化学和制霉菌素穿孔膜片钳技术研究了瞬时受体电位香草酸亚家族成员1（TRPV1）通道（其本质上有助于疼痛感觉的检测）在大鼠成牙本质细胞中的表达。免疫组织化学观察显示TRPV1免疫反应定位于成牙本质细胞膜的远端区域。在膜片钳实验中，我们观察到辣椒素诱导的内向电流，该电流被TRPV1通道拮抗剂辣椒素阻断。我们的结果表明TRPV1通道在成牙本质细胞中有显著表达，这表明成牙本质细胞可能直接对诸如热刺激等有害刺激作出反应，并指出有必要基于成牙本质细胞中的跨膜离子信号重新考虑牙本质感觉的细胞机制。
