The tectorial membrane (TM) is an extracellular matrix situated over the sensory cells of the cochlea. Its strategic location, together with the results of recent TM-specific mutation studies, suggests that it has an important role in the mechanism by which the cochlea transduces mechanical energy into neural excitation. A detailed characterization of TM mechanical properties is fundamental to understanding its role in cochlear mechanics. In this work, the mechanical properties of the TM are characterized in the radial and longitudinal directions using nano-and microindentation experiments conducted by using atomic force spectroscopy. We find that the stiffness in the main body region and in the spiral limbus attachment zone does not change significantly along the length of the cochlea. The main body of the TM is the softest region, whereas the spiral limbus attachment zone is stiffer, with the two areas having averaged Young's modulus values of 37 ؎ 3 and 135 ؎ 14 kPa, respectively. By contrast, we find that the stiffness of the TM in the region above the outer hair cells (OHCs) increases by one order of magnitude in the longitudinal direction, from 24 ؎ 4 kPa in the apical region to 210 ؎ 15 kPa at the basilar end of the TM. Scanning electron microscopy analysis shows differences in the collagen fiber arrangements in the OHC zone of the TM that correspond to the observed variations in mechanical properties. The longitudinal increase in TM stiffness is similar to that found for the OHC stereocilia, which supports the existence of mechanical coupling between these two structures.cochlea ͉ collagen fibers ͉ indentation ͉ hearing T he tectorial membrane (TM) is a heterogeneous and gelatinous extracellular matrix. It is located in the cochlea, which transduces mechanical audio stimuli into an electrical signal. Under physiological conditions, 97% of the weight of the TM is water, whereas the remainder is composed of proteins and protoglycans (1). Nearly half of these proteins are collagens, principally of type II, which form fibrils that are assembled along the radial direction (Fig. 1A); at the surface of the TM, which faces away from the hair-cells, they form a mesh-like structure called the covering net.Structurally, the TM spans the entire length of the cochlea and is Ϸ100 m wide and 50 m thick. It is strategically situated over the sensory cells of the cochlea: the outer (OHCs) and inner (IHCs) hair cells (Fig. 1B). The electromotility of OHCs is thought to play a central role in the cochlear mechanicalelectrical transduction process (2, 3), whereas IHCs synapse directly with the auditory nerve (4). Upon auditory stimulation, deflection of the stereocilium bundles, which exist both in OHCs and IHCs, directly converts the mechanical energy into an electrical signal. This conversion is the physiological function of these cells. An additional function of the OHCs is electromechanical transduction. Whereas the stereocilia of OHCs are physically embedded in the lower surface of the TM, the stereocilia of the IHC ar...

Shining light on local order: The relations between local crystalline order and peak intensities in the infrared spectra of calcite are explained in terms of different sensitivities to CaO and O⋅⋅⋅O distances (see picture) by comparing ab initio phonon spectra for ideal and distorted calcite unit cells with experimental spectra of various biogenic and geological calcites.

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The exceptional performance of mammalian hearing is due to the cochlea's amplification of sound-induced mechanical stimuli. During acoustic stimulation, the vertical motion of the outer hair cells relative to the tectorial membrane (TM) is converted into the lateral motion of their stereocilia. The actual mode of this conversion, which represents a fundamental step in hearing, remains enigmatic, as it is unclear why the stereocilia are deflected when pressed against the TM, rather than penetrating it. In this study we show that deflection of the stereocilia is a direct outcome of the anisotropic material properties of the TM. Using force spectroscopy, we find that the vertical stiffness of the TM is significantly larger than its lateral stiffness. As a result, the TM is more resistant to the vertical motion of stereocilia than to their lateral motion, and so they are deflected laterally when pushed against the TM. Our findings are confirmed by finite element simulations of the mechanical interaction between the TM and stereocilia, which show that the vertical outer hair cells motion is converted into lateral stereocilia motion when the experimentally determined stiffness values are incorporated into the model. Our results thus show that the material properties of the TM play a central and previously unknown role in mammalian hearing.

The tectorial membrane (TM) is an extracellular matrix of the cochlea whose prominent role in hearing has been demonstrated through mutation studies. The C1509G mutation of the Tecta gene, which encodes for the α-tectorin protein, leads to hearing loss. The heterozygote TM only attaches to the first row of outer hair cells (OHCs), and the homozygote TM does not attach to any OHCs. Here we measured the morphology and mechanical properties of wild-type, heterozygous, and homozygous Tecta TMs. Morphological analyses conducted with second- and third-harmonic imaging, scanning electron microscopy, and immunolabeling revealed marked changes in the collagen architecture and stereocilin-labeling patterns of the mutant TMs. The mechanical properties of the mutant TM were measured by force spectroscopy. Whereas the axial Young's modulus of the low-frequency (apical) region of Tecta mutant TM samples was similar to that of wild-type TMs, it significantly decreased in the basal region to a value approaching that found at the apex. Modeling simulations suggest that a reduced TM Young's modulus is likely to reduce OHC stereociliary deflection. These findings argue that the heterozygote C1509G mutation results in a lack of attachment of the TM to the OHCs, which in turn reduces both the overall number of OHCs that are involved in mechanotransduction and the degree of mechanotransduction exhibited by the OHCs that remain attached to the TM.