Mechanically induced length changes of isolated outer hair cells are metabolically dependent.
ABSTRACT Isolated outer hair cells from the organ of Corti of the guinea pig have been shown to change length in response to a mechanical stimulus in the form of a tone burst at a fixed frequency of 200 Hz (Canlon et al., 1988). In the present study, the threshold of movement for individual outer hair cells is related to the original length of the cell such that long cells are more sensitive than short cells for all cochlear locations studied. Length changes could be elicited when the stimulus was projected at any site along the longitudinal axis of the plasma membrane. Length changes were not elicited when the stereocilia were stimulated directly. These mechanically-induced length changes were found to be metabolically dependent. In the presence of either sodium cyanide or 2,4-dinitrophenol, the motile response of outer hair cells was completely blocked within 30 min. When the extracellular pH was altered in a graded fashion, the motile response decreased gradually. Furthermore, 3 microM poly-L-lysine or poly-D-lysine of different molecular weights were also effective in blocking the motile response, whereas the negatively charged polyaminoacid, poly-L-aspartate, was not effective. Fluorescently-labelled poly-lysine demonstrated that the plasma membrane, stereocilia, and nucleus were the most intensely stained structures of the outer hair cells. It is suggested that the passive influx of poly-lysine is responsible for the inhibition of the motile response. Finally, the finding that the bidirectional motile response of isolated outer hair cells induced by mechanical stimulation is dependent on the metabolic state of the cell distinguishes this type of motility from the electrically induced outer hair cell shape changes.
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ABSTRACT: The outer hair cells of the cochlea occur in three distinct and geometrically precise rows and, unusually, display both sensing and motor properties. As well as sensing sound, outer hair cells (OHCs) undergo cycle-by-cycle length changes in response to stimulation. OHCs are central to the way in which the cochlea processes and amplifies sounds, but how they do so is presently unknown. In explanation, this paper proposes that outer hair cells act like a single-port surface acoustic wave (SAW) resonator in which the interdigital electrodes--the three distinctive rows--exhibit the required electromechanical and mechanoelectrical properties. Thus, frequency analysis in the cochlea might occur through sympathetic resonance of a bank of interacting cells whose microscopic separation largely determines the resonance frequency. In this way, the cochlea could be tuned from 20 Hz at the apex, where the spacing is largest, to 20 kHz at the base, where it is smallest. A suitable candidate for a wave that could mediate such a short-wavelength interaction--a 'squirting wave' known in ultrasonics--has recently been described. Such a SAW resonator could thereby underlie the 'cochlear amplifier'--the device whose action is evident to auditory science but whose identity has not yet been established.Bioinspiration & Biomimetics 10/2006; 1(3):96-101. · 2.41 Impact Factor
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ABSTRACT: The mammalian outer hair cells (OHCs) are mechanical effectors of the cochlea. The slow motility of OHCs is considered to be a possible adaptive mechanism in the cochlea. It is suggested that passive calcium-independent slow motility induced by hyposmotic activation may have physiological or pathological significance even in normal or impaired hearing of cochlear origin. The cell swelling induced by hyposmotic stimulation has been shown to be accompanied by an increase of intracellular Ca2+ concentrations ([Ca2+]i) in OHCs. This [Ca2+]i increase may subsequently activate metabolic processes including phosphorylation in OHCs. Therefore, the ionic environment and the changes in osmolarity of the inner ear may affect the OHC motility, thereby varying the sensitivity of the inner ear to the sound. The functional expression of transient receptor potential vanilloid 4 (TRPV4) is involved in the hypotonic stimulation-induced Ca2+ influx in OHCs. It is suggested that TRPV4 may function as an osmo- and mechanosensory receptor in OHCs. Recent study showed that hyposmotic stimulation can induce nitric oxide (NO) production by the [Ca2+]i increase, which is presumably mediated by the activation of TRPV4 in OHCs. NO conversely inhibits the Ca2+ response via the NO-cGMP-PKG pathway by a feedback mechanism. Any disturbance in the homeostasis of inner ear fluids may therefore affect the functional properties of OHCs by NO via the activation of TRPV4, thereby influencing the delivery of auditory information. In this review, volume regulation in OHCs also will be discussed.12/2008: pages 115-131;
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ABSTRACT: The mammalian Slc4 (Solute carrier 4) family of transporters is a functionally diverse group of 10 multi-spanning membrane proteins that includes three Cl-HCO3 exchangers (AE1-3), five Na(+)-coupled HCO3(-) transporters (NCBTs), and two other unusual members (AE4, BTR1). In this review, we mainly focus on the five mammalian NCBTs-NBCe1, NBCe2, NBCn1, NDCBE, and NBCn2. Each plays a specialized role in maintaining intracellular pH and, by contributing to the movement of HCO3(-) across epithelia, in maintaining whole-body pH and otherwise contributing to epithelial transport. Disruptions involving NCBT genes are linked to blindness, deafness, proximal renal tubular acidosis, mental retardation, and epilepsy. We also review AE1-3, AE4, and BTR1, addressing their relevance to the study of NCBTs. This review draws together recent advances in our understanding of the phylogenetic origins and physiological relevance of NCBTs and their progenitors. Underlying these advances is progress in such diverse disciplines as physiology, molecular biology, genetics, immunocytochemistry, proteomics, and structural biology. This review highlights the key similarities and differences between individual NCBTs and the genes that encode them and also clarifies the sometimes confusing NCBT nomenclature.Physiological Reviews 04/2013; 93(2):803-959. · 30.17 Impact Factor