Dewey James B
Caruso Department of Otolaryngology - Head & Neck Surgery, Keck School of Medicine, University of Southern California, Los Angeles, CA 90033, USA.
bioRxiv. 2024 Dec 20:2024.12.19.629412. doi: 10.1101/2024.12.19.629412.
Cochlear outer hair cells (OHCs) transduce sound-induced vibrations of their stereociliary bundles into receptor potentials that drive changes in cell length. While fast, phasic OHC length changes are thought to underlie an amplification process required for sensitive hearing, OHCs also exhibit large tonic length changes. The origins and functional significance of this tonic motility are unclear. Here, cochlear vibration measurements reveal tonic, sound-induced OHC motility in mice with stereociliary defects that impair mechanotransduction and eliminate cochlear amplification. Tonic motility in impaired mice was physiologically vulnerable but weakly related to any residual phasic motility, possibly suggesting a dissociation between the underlying mechanisms. Nevertheless, a simple model demonstrates how tonic responses in both normal and impaired mice can result from asymmetric mechanotransduction currents and be large even when phasic motility is undetectable. Tonic OHC responses are therefore not unique to sensitive ears, though their potential functional role remains uncertain.
耳蜗外毛细胞（OHCs）将其静纤毛束的声音诱导振动转化为驱动细胞长度变化的受体电位。虽然快速的、相位性的OHC长度变化被认为是灵敏听力所需放大过程的基础，但OHCs也表现出较大的紧张性长度变化。这种紧张性运动的起源和功能意义尚不清楚。在这里，耳蜗振动测量揭示了在具有损害机械转导并消除耳蜗放大作用的静纤毛缺陷的小鼠中，声音诱导的紧张性OHC运动。受损小鼠的紧张性运动在生理上很脆弱，但与任何残余的相位性运动弱相关，这可能表明潜在机制之间存在分离。然而，一个简单的模型展示了正常和受损小鼠中的紧张性反应如何由不对称的机械转导电流产生，并且即使在无法检测到相位性运动时也可能很大。因此，紧张性OHC反应并非灵敏耳朵所特有，尽管它们潜在的功能作用仍不确定。
