Department of Surgery-Otolaryngology, University of Kentucky Medical Center, Lexington, Kentucky, United States of America.
PLoS One. 2009 Nov 20;4(11):e7923. doi: 10.1371/journal.pone.0007923.
Outer hair cell (OHC) or prestin-based electromotility is an active cochlear amplifier in the mammalian inner ear that can increase hearing sensitivity and frequency selectivity. In situ, Deiters supporting cells are well-coupled by gap junctions and constrain OHCs standing on the basilar membrane. Here, we report that both electrical and mechanical stimulations in Deiters cells (DCs) can modulate OHC electromotility. There was no direct electrical conductance between the DCs and the OHCs. However, depolarization in DCs reduced OHC electromotility associated nonlinear capacitance (NLC) and distortion products. Increase in the turgor pressure of DCs also shifted OHC NLC to the negative voltage direction. Destruction of the cytoskeleton in DCs or dissociation of the mechanical-coupling between DCs and OHCs abolished these effects, indicating the modulation through the cytoskeleton activation and DC-OHC mechanical coupling rather than via electric field potentials. We also found that changes in gap junctional coupling between DCs induced large membrane potential and current changes in the DCs and shifted OHC NLC. Uncoupling of gap junctions between DCs shifted NLC to the negative direction. These data indicate that DCs not only provide a physical scaffold to support OHCs but also can directly modulate OHC electromotility through the DC-OHC mechanical coupling. Our findings reveal a new mechanism of cochlear supporting cells and gap junctional coupling to modulate OHC electromotility and eventually hearing sensitivity in the inner ear.
外毛细胞（OHC）或 prestin 为基础的电活动是哺乳动物内耳中的一种主动耳蜗放大器，可提高听力灵敏度和频率选择性。在原位，Deiters 支持细胞通过缝隙连接紧密连接，并限制基底膜上的 OHC。在这里，我们报告说，Deiters 细胞（DC）的电刺激和机械刺激都可以调节 OHC 的电活动。DC 和 OHC 之间没有直接的电导率。然而，DC 的去极化降低了与 OHC 非线性电容（NLC）和失真产物相关的电活动。DC 膨压的增加也将 OHC 的 NLC 移至负电压方向。DC 细胞骨架的破坏或 DC 和 OHC 之间机械耦联的解离消除了这些影响，表明这种调制是通过细胞骨架激活和 DC-OHC 机械耦联而不是通过电场势来实现的。我们还发现，DC 之间缝隙连接耦联的变化引起了 DC 中的大膜电位和电流变化，并改变了 OHC 的 NLC。DC 之间缝隙连接的解耦将 NLC 移至负方向。这些数据表明，DC 不仅为 OHC 提供了物理支架，而且还可以通过 DC-OHC 机械耦联直接调节 OHC 的电活动。我们的发现揭示了耳蜗支持细胞和缝隙连接耦联调节 OHC 电活动，最终调节内耳听力敏感性的新机制。
