Regulation of outer hair cell cytoskeletal stiffness by intracellular Ca2+:: underlying mechanism and implications for cochlear mechanics

被引:40
作者
Frolenkov, GI
Mammano, F
Kachar, B
机构
[1] NIDCD, Sect Struct Cell Biol, NIH, Bethesda, MD 20892 USA
[2] Ist Nazl Fis Mat, Padua, Italy
[3] Venetian Inst Mol Med, Padua, Italy
关键词
cochlear amplifier; prestin; olivocohlear bundle; acetylcholine; intracellular calcium stores; slow motility;
D O I
10.1016/S0143-4160(02)00228-2
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
Two Ca2+-dependent mechanisms have been proposed to regulate the mechanical properties of outer hair cells (OHCs), the sensory-motor receptors of the mammalian cochlea. One involves the efferent neurotransmitter, acetylcholine, decreasing OHC axial stiffness. The other depends on elevation of intracellular free Ca2+ concentration ([Ca2+](i)) resulting in OHC elongation, a process known as Ca2+-dependent slow motility. Here we provide evidence that both these phenomena share a common mechanism. In whole-cell patch-clamp conditions, a fast increase of [Ca2+](i) by UV-photolysis of caged Ca2+ or by extracellular application of Ca2+-ionophore, ionomycin, produced relatively slow (time constant similar to20 s) cell elongation. When OHCs were partially collapsed by applying minimal negative pressure through the patch pipette, elevation of the [Ca2+](i) up to millimole levels (estimated by Fura-2) was unable to restore the cylindrical shape of the OHC. Stiffness measurements with vibrating elastic probes showed that the increase of [Ca2+], causes a decrease of OHC axial stiffness, with time course similar to that of the Ca2+-dependent elongation, without developing any measurable force. We concluded that, contrary to a previous proposal, Ca2+-induced OHC elongation is unlikely to be driven by circumferential contraction of the lateral wall, but is more likely a passive mechanical reaction of the turgid OHC to Ca2+-induced decrease of axial stiffness. This may be the key phenomenon for controlling gain and operating point of the cochlear amplifier. (C) 2003 Elsevier Science Ltd. All rights reserved.
引用
收藏
页码:185 / 195
页数:11
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