Journal articles: 'Outer hair cells'

1

Ashmore, Jonathan. "Outer Hair Cells and Electromotility." Cold Spring Harbor Perspectives in Medicine 9, no. 7 (September 4, 2018): a033522. http://dx.doi.org/10.1101/cshperspect.a033522.

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Ashmore, Jonathan. "Cochlear Outer Hair Cell Motility." Physiological Reviews 88, no. 1 (January 2008): 173–210. http://dx.doi.org/10.1152/physrev.00044.2006.

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Normal hearing depends on sound amplification within the mammalian cochlea. The amplification, without which the auditory system is effectively deaf, can be traced to the correct functioning of a group of motile sensory hair cells, the outer hair cells of the cochlea. Acting like motor cells, outer hair cells produce forces that are driven by graded changes in membrane potential. The forces depend on the presence of a motor protein in the lateral membrane of the cells. This protein, known as prestin, is a member of a transporter superfamily SLC26. The functional and structural properties of prestin are described in this review. Whether outer hair cell motility might account for sound amplification at all frequencies is also a critical question and is reviewed here.

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Gummer, Anthony W., Jens Meyer, Gerhard Frank, Marc P. Scherer, and Serena Preyer. "Mechanical Transduction in Outer Hair Cells." Audiology and Neurotology 7, no. 1 (2002): 13–16. http://dx.doi.org/10.1159/000046856.

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Zenner, Hans Peter. "Motile responses in outer hair cells." Hearing Research 22, no. 1-3 (January 1986): 83–90. http://dx.doi.org/10.1016/0378-5955(86)90082-1.

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Prieto, J., J. A. Merchán, P. Gil-Loyzaga, and J. Rueda. "Subsurface material in outer hair cells." Hearing Research 21, no. 3 (1986): 277–80. http://dx.doi.org/10.1016/0378-5955(86)90225-x.

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Stauffer, Eric A., and Jeffrey R. Holt. "Sensory Transduction and Adaptation in Inner and Outer Hair Cells of the Mouse Auditory System." Journal of Neurophysiology 98, no. 6 (December 2007): 3360–69. http://dx.doi.org/10.1152/jn.00914.2007.

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Auditory function in the mammalian inner ear is optimized by collaboration of two classes of sensory cells known as inner and outer hair cells. Outer hair cells amplify and tune sound stimuli that are transduced and transmitted by inner hair cells. Although they subserve distinct functions, they share a number of common properties. Here we compare the properties of mechanotransduction and adaptation recorded from inner and outer hair cells of the postnatal mouse cochlea. Rapid outer hair bundle deflections of about 0.5 micron evoked average maximal transduction currents of about 325 pA, whereas inner hair bundle deflections of about 0.9 micron were required to evoke average maximal currents of about 310 pA. The similar amplitude was surprising given the difference in the number of stereocilia, 81 for outer hair cells and 48 for inner hair cells, but may be reconciled by the difference in single-channel conductance. Step deflections of inner and outer hair bundles evoked adaptation that had two components: a fast component that consisted of about 60% of the response occurred over the first few milliseconds and a slow component that consisted of about 40% of the response followed over the subsequent 20–50 ms. The rate of the slow component in both inner and outer hair cells was similar to the rate of slow adaptation in vestibular hair cells. The rate of the fast component was similar to that of auditory hair cells in other organisms and several properties were consistent with a model that proposes calcium-dependent release of tension allows transduction channel closure.

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Jia, Shuping, and David Z. Z. He. "Motility-associated hair-bundle motion in mammalian outer hair cells." Nature Neuroscience 8, no. 8 (July 24, 2005): 1028–34. http://dx.doi.org/10.1038/nn1509.

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8

Biswas, Joyshree, Robert S. Pijewski, Rohit Makol, Tania G. Miramontes, Brianna L. Thompson, Lyndsay C. Kresic, Alice L. Burghard, Douglas L. Oliver, and David C. Martinelli. "C1ql1 is expressed in adult outer hair cells of the cochlea in a tonotopic gradient." PLOS ONE 16, no. 5 (May 12, 2021): e0251412. http://dx.doi.org/10.1371/journal.pone.0251412.

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Hearing depends on the transduction of sounds into neural signals by the inner hair cells of the cochlea. Cochleae also have outer hair cells with unique electromotile properties that increase auditory sensitivity, but they are particularly susceptible to damage by intense noise exposure, ototoxic drugs, and aging. Although the outer hair cells have synapses on afferent neurons that project to the brain, the function of this neuronal circuit is unclear. Here, we created a novel mouse allele that inserts a fluorescent reporter at the C1ql1 locus which revealed gene expression in the outer hair cells and allowed creation of outer hair cell-specific C1ql1 knockout mice. We found that C1ql1 expression in outer hair cells corresponds to areas with the most sensitive frequencies of the mouse audiogram, and that it has an unexpected adolescence-onset developmental timing. No expression was observed in the inner hair cells. Since C1QL1 in the brain is made by neurons, transported anterogradely in axons, and functions in the synaptic cleft, C1QL1 may serve a similar function at the outer hair cell afferent synapse. Histological analyses revealed that C1ql1 conditional knockout cochleae may have reduced outer hair cell afferent synapse maintenance. However, auditory behavioral and physiological assays did not reveal a compelling phenotype. Nonetheless, this study identifies a potentially useful gene expressed in the cochlea and opens the door for future studies aimed at elucidating the function of C1QL1 and the function of the outer hair cell and its afferent neurons.

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Chertoff, M. E., and W. E. Brownell. "Characterization of cochlear outer hair cell turgor." American Journal of Physiology-Cell Physiology 266, no. 2 (February 1, 1994): C467—C479. http://dx.doi.org/10.1152/ajpcell.1994.266.2.c467.

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The cochlear outer hair cell (OHC) is a cylindrical cell with structural features suggestive of a hydraulic skeleton, i.e., an elastic shell with a positive internal pressure. This study characterizes the role of the OHC elevated cytoplasmic pressure in maintaining the cell shape. Intracellular pressure of OHCs from guinea pig is estimated by measuring changes in cell morphology in response to increasing or decreasing osmolarity. Cells collapse when subjected to a continuous increase in osmolarity. Collapse occurs at an average of 8 mosM above the standard medium, suggesting that normal cells have an effective intracellular pressure of 128 mmHg. Fewer cells collapse when exposed to slow rates of osmolarity increase than cells exposed to fast rates of osmolarity increase, although the final change in osmolarity in the perfusion chamber is similar. Furthermore, cells undergo a slow, spontaneous increase in volume on exposure to either no osmolarity change or slow rates of osmolarity increase, suggesting that the cell's internal osmolarity increases in vitro. After volume reduction or elevation, cells do not return to their initial volume.

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Wada, Hiroshi. "Mechanics of inner and outer hair cells." AUDIOLOGY JAPAN 59, no. 3 (2016): 161–69. http://dx.doi.org/10.4295/audiology.59.161.

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11

Ashmore, Jonathan F. "Active cochlear mechanics and outer hair cells." Journal of the Acoustical Society of America 143, no. 3 (March 2018): 1809. http://dx.doi.org/10.1121/1.5035927.

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12

Wu, Tao, Sripriya Ramamoorthy, Teresa Wilson, Fangyi Chen, Edward Porsov, Hrebesh Subhash, Sarah Foster, et al. "Optogenetic Control of Mouse Outer Hair Cells." Biophysical Journal 110, no. 2 (January 2016): 493–502. http://dx.doi.org/10.1016/j.bpj.2015.11.3521.

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13

Dallos, Peter. "Cochlear amplification, outer hair cells and prestin." Current Opinion in Neurobiology 18, no. 4 (August 2008): 370–76. http://dx.doi.org/10.1016/j.conb.2008.08.016.

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14

Crist, Jennifer R., Maureen Fallon, and Richard P. Bobbin. "Volume regulation in cochlear outer hair cells." Hearing Research 69, no. 1-2 (September 1993): 194–98. http://dx.doi.org/10.1016/0378-5955(93)90107-c.

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15

Iwasa, Kuni H. "Kinetic Membrane Model of Outer Hair Cells." Biophysical Journal 120, no. 1 (January 2021): 122–32. http://dx.doi.org/10.1016/j.bpj.2020.11.017.

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16

Fu, Mingyu, Mengzi Chen, Xiao Yan, Xueying Yang, Jinfang Xiao, and Jie Tang. "The Effects of Urethane on Rat Outer Hair Cells." Neural Plasticity 2016 (2016): 1–11. http://dx.doi.org/10.1155/2016/3512098.

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The cochlea converts sound vibration into electrical impulses and amplifies the low-level sound signal. Urethane, a widely used anesthetic in animal research, has been shown to reduce the neural responses to auditory stimuli. However, the effects of urethane on cochlea, especially on the function of outer hair cells, remain largely unknown. In the present study, we compared the cochlear microphonic responses between awake and urethane-anesthetized rats. The results revealed that the amplitude of the cochlear microphonic was decreased by urethane, resulting in an increase in the threshold at all of the sound frequencies examined. To deduce the possible mechanism underlying the urethane-induced decrease in cochlear sensitivity, we examined the electrical response properties of isolated outer hair cells using whole-cell patch-clamp recording. We found that urethane hyperpolarizes the outer hair cell membrane potential in a dose-dependent manner and elicits larger outward current. This urethane-induced outward current was blocked by strychnine, an antagonist of theα9 subunit of the nicotinic acetylcholine receptor. Meanwhile, the function of the outer hair cell motor protein, prestin, was not affected. These results suggest that urethane anesthesia is expected to decrease the responses of outer hair cells, whereas the frequency selectivity of cochlea remains unchanged.

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Cortese, Matteo, Samantha Papal, Francisco Pisciottano, Ana Belén Elgoyhen, Jean-Pierre Hardelin, Christine Petit, Lucia Florencia Franchini, and Aziz El-Amraoui. "Spectrin βV adaptive mutations and changes in subcellular location correlate with emergence of hair cell electromotility in mammalians." Proceedings of the National Academy of Sciences 114, no. 8 (February 8, 2017): 2054–59. http://dx.doi.org/10.1073/pnas.1618778114.

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The remarkable hearing capacities of mammals arise from various evolutionary innovations. These include the cochlear outer hair cells and their singular feature, somatic electromotility, i.e., the ability of their cylindrical cell body to shorten and elongate upon cell depolarization and hyperpolarization, respectively. To shed light on the processes underlying the emergence of electromotility, we focused on the βV giant spectrin, a major component of the outer hair cells' cortical cytoskeleton. We identified strong signatures of adaptive evolution at multiple sites along the spectrin-βV amino acid sequence in the lineage leading to mammals, together with substantial differences in the subcellular location of this protein between the frog and the mouse inner ear hair cells. In frog hair cells, spectrin βV was invariably detected near the apical junctional complex and above the cuticular plate, a dense F-actin meshwork located underneath the apical plasma membrane. In the mouse, the protein had a broad punctate cytoplasmic distribution in the vestibular hair cells, whereas it was detected in the entire lateral wall of cochlear outer hair cells and had an intermediary distribution (both cytoplasmic and cortical, but restricted to the cell apical region) in cochlear inner hair cells. Our results support a scenario where the singular organization of the outer hair cells’ cortical cytoskeleton may have emerged from molecular networks initially involved in membrane trafficking, which were present near the apical junctional complex in the hair cells of mammalian ancestors and would have subsequently expanded to the entire lateral wall in outer hair cells.

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18

Knirsch, M., N. Brandt, C. Braig, S. Kuhn, B. Hirt, S. Munkner, M. Knipper, and J. Engel. "Persistence of Cav1.3 Ca2+ Channels in Mature Outer Hair Cells Supports Outer Hair Cell Afferent Signaling." Journal of Neuroscience 27, no. 24 (June 13, 2007): 6442–51. http://dx.doi.org/10.1523/jneurosci.5364-06.2007.

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19

Ramírez-Camacho, R., J. R. García-Berrocal, A. Trinidad, J. M. Verdaguer, and J. Nevado. "Blebs in inner and outer hair cells: a pathophysiological hypothesis." Journal of Laryngology & Otology 122, no. 11 (January 10, 2008): 1151–55. http://dx.doi.org/10.1017/s002221510700134x.

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AbstractIntroduction:The ototoxic effects of cisplatin include loss of outer hair cells, degeneration of the stria vascularis and a decrease in the number of spiral ganglion cells. Scanning microscopy has shown balloon-like protrusions (blebs) of the plasma membrane of inner hair cells following cisplatin administration. The present study was undertaken to identify the possible role of inner and outer hair cell blebs in the pathogenesis of cisplatin-induced ototoxicity.Materials and methods:Twenty-five guinea pigs were injected with cisplatin and their hearing tested at different time-points, before sacrifice and examination with scanning electron microscopy.Results and analysis:Seven animals showed blebs in the inner hair cells at different stages. Hearing thresholds were lower in animals showing blebs.Discussion:Cisplatin seems to be able to induce changes in inner hair cells as well as in other structures in the organ of Corti. Blebbing observed in animals following cisplatin administration could play a specific role in the regulation of intracellular pressure.

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20

Schwartz, Ilsa, Chong-Sun Kim, and See-Ok Shin. "Ultrastructural Changes in the Cochlea of the Guinea Pig after Fast Neutron Irradiation." Otolaryngology–Head and Neck Surgery 110, no. 4 (April 1994): 419–27. http://dx.doi.org/10.1177/019459989411000412.

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Guinea pigs were irradiated with fast neutrons. After a single dose of 2, 6, 10, or 15 Gy was applied, scanning and transmission electron microscopy of the temporal bone was performed to assess the effect of fast neutron irradiation on the cochlea. Outer hair cell damage appeared with neutron irradiation of more than 10 Gy, and Inner hair cell damage with neutron Irradiation of more than 15 Gy. Outer hair cells were more severely damaged than Inner hair cells. No statistically significant differences were found in damage of basal, middle, and apical turns. The second and third rows of outer hair cells were more severely damaged than the first row of outer hair cells. The most significant findings in transmission electron microscopy were clumping of chromatin and extension of the heterochromatin in the nuclei of hair cells. The cytoplasmic changes were sequestration of cytoplasm, various changes of mitochondria, formation of vacuoles, and irregularly arranged stereocilia. The morphologic change in stria vascularis was intercellular and perivascular fluid accumulation. It appeared to be a reversible process.

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Meyer, Jens, Andreas F. Mack, and Anthony W. Gummer. "Pronounced infracuticular endocytosis in mammalian outer hair cells." Hearing Research 161, no. 1-2 (November 2001): 10–22. http://dx.doi.org/10.1016/s0378-5955(01)00338-0.

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22

Géléoc, Gwénaëlle S. G., and Jeffrey R. Holt. "Auditory amplification: outer hair cells pres the issue." Trends in Neurosciences 26, no. 3 (March 2003): 115–17. http://dx.doi.org/10.1016/s0166-2236(03)00030-4.

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23

Zheng, Jing, Laird D. Madison, Dominik Oliver, Bernd Fakler, and Peter Dallos. "Prestin, the Motor Protein of Outer Hair Cells." Audiology and Neurotology 7, no. 1 (2002): 9–12. http://dx.doi.org/10.1159/000046855.

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Magdolna Szõnyi, Péter Csermely, Is. "Acetylcholine-induced Phosphorylation in Isolated Outer Hair Cells." Acta Oto-Laryngologica 119, no. 2 (January 1999): 185–88. http://dx.doi.org/10.1080/00016489950181639.

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25

Kachar, Bechara, William E. Brownell, Richard Altschuler, and Jörgen Fex. "Electrokinetic shape changes of cochlear outer hair cells." Nature 322, no. 6077 (July 1986): 365–68. http://dx.doi.org/10.1038/322365a0.

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26

Holley, M. C., and J. F. Ashmore. "A cytoskeletal spring in cochlear outer hair cells." Nature 335, no. 6191 (October 1988): 635–37. http://dx.doi.org/10.1038/335635a0.

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Bohne, Barbara A., Gary W. Harding, and Steve C. Lee. "Death pathways in noise-damaged outer hair cells." Hearing Research 223, no. 1-2 (January 2007): 61–70. http://dx.doi.org/10.1016/j.heares.2006.10.004.

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Lu, Timothy K., Serhii Zhak, Peter Dallos, and Rahul Sarpeshkar. "Fast cochlear amplification with slow outer hair cells." Hearing Research 214, no. 1-2 (April 2006): 45–67. http://dx.doi.org/10.1016/j.heares.2006.01.018.

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Nadol, Joseph B., and Barbara J. Burgess. "Morphology of Synapses at the Base of Hair Cells in the Organ of Corti of the Chimpanzee." Annals of Otology, Rhinology & Laryngology 99, no. 3 (March 1990): 215–20. http://dx.doi.org/10.1177/000348949009900311.

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The synaptic morphology of inner and outer hair cells of the organ of Corti of the chimpanzee was evaluated by serial section electron microscopy. The morphology of nerve terminals and synapses at both sites was very similar to that of human and other mammalian species. Two types of nerve terminals, nonvesiculated and vesiculated, with distinct synaptic morphology were found. In addition, between some nonvesiculated endings and outer hair cells, a reciprocal synaptic relationship was seen. In such terminals there was morphologic evidence for transmission from hair cell to neuron and from neuron to hair cell between a single neuron and an outer hair cell.

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Khanna, Shyam M., Mats Ulfendahl, and Åke Flock. "Mechanical Tuning Characteristics of Outer Hair Cells and Hensen's Cells." Acta Oto-Laryngologica 108, sup467 (January 1989): 139–44. http://dx.doi.org/10.3109/00016488909138330.

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Murakoshi, Michio, and Hiroshi Wada. "GS1-30 SOUND AMPLIFICATION MECHANISM BY THREE ROWS OF OUTER HAIR CELLS IN MAMMALS(GS1: Cell and Tissue Biomechanics VI)." Proceedings of the Asian Pacific Conference on Biomechanics : emerging science and technology in biomechanics 2015.8 (2015): 141. http://dx.doi.org/10.1299/jsmeapbio.2015.8.141.

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Witt, C. M., H. Y. Hu, W. E. Brownell, and D. Bertrand. "Physiologically silent sodium channels in mammalian outer hair cells." Journal of Neurophysiology 72, no. 2 (August 1, 1994): 1037–40. http://dx.doi.org/10.1152/jn.1994.72.2.1037.

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1. Voltage-dependent properties of isolated guinea pig outer hair cells (OHCs) were investigated using whole-cell recording. An inward current was detected in approximately 10% of the cells. This inward current was identified as belonging to the voltage-activated sodium current family on the basis of its high sensitivity to tetrodotoxin and the effect of substitution of impermeant ions. Although this is the first report of a sodium current in the mammalian cochlea, it differs from the classical neuronal sodium current by having a variable magnitude from cell to cell and an inactivation that is shifted to hyperpolarized potentials. The sensory processing role of hair cells in general and outer hair cells in particular could be disrupted by the presence of a regenerative voltage-dependent current. The functional role of the OHC sodium channels is puzzling, particularly as they may be silent in vivo.

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Yi, Li, and He David Z. "The Cochlear Amplifier: Is it Hair Bundle Motion of Outer Hair Cells?" Journal of Otology 9, no. 2 (June 2014): 64–72. http://dx.doi.org/10.1016/s1672-2930(14)50017-7.

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34

Ohnishi, S., M. Hara, M. Inoue, T. Yamashita, T. Kumazawa, A. Minato, and C. Inagaki. "Delayed shortening and shrinkage of cochlear outer hair cells." American Journal of Physiology-Cell Physiology 263, no. 5 (November 1, 1992): C1088—C1095. http://dx.doi.org/10.1152/ajpcell.1992.263.5.c1088.

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Slow shortening of cochlear outer hair cells has been speculated to modify cochlear sensitivity. Tetanic electrical field stimulation of isolated outer hair cells from guinea pigs shortened the cells for 2-3 min. Electrical stimulation reduced cell length and volume (-13.5 +/- 1.5 and -37.3 +/- 3.0% of initial values, respectively, n = 16) and decreased the intracellular Cl- concentration. Cytochalasin B (100 microM) inhibited electrical stimulation-induced shortening but not volume reduction. The following chemicals or manipulations inhibited the responses: 10 microM furosemide, 0.1 mM 4,4'-diisothiocyanostilbene-2,2'-disulfonic acid (DIDS), 1 mM anthracene-9-carboxylic acid (AC9), 25 mM tetraethylammonium, 2.3 microM charybdotoxin (ChTX), 250 nM omega-conotoxin, and Ca(2+)-free medium. These findings suggest that both electrical stimulation-induced shortening and shrinkage of outer hair cells result not only from an actin-mediated contractile force, but also from Cl- efflux through furosemide-, DIDS-, and AC9-sensitive Cl- channels, and K+ efflux through ChTX-sensitive K+ channels.

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Chole, Richard A., and Maggie Chiu. "Cochlear Hair Cell Stereocilia Loss in LP/J Mice with Bone Dysplasia of the Middle Ear." Annals of Otology, Rhinology & Laryngology 98, no. 6 (June 1989): 461–65. http://dx.doi.org/10.1177/000348948909800613.

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LP/J inbred mice spontaneously develop bony lesions of the middle ear and otic capsule that are similar to those of human otosclerosis and tympanosclerosis. These mice also have progressive loss of hearing due to cochlear hair cell loss. The purpose of this study was to describe quantitatively the deterioration and loss of cochlear hair cells to serve as a basis for future experiments attempting to alter the course of this disorder. Cochleas from 37 LP/J inbred mice were examined by scanning electron microscopy. The stereocilia loss in the cochlea was evident as early as 15 weeks of age and progressed from the basal turn to the apex. Outer hair cells were affected more than inner hair cells. As outer hair cells deteriorated we observed fusion, bending, and breakage of stereocilia. There were no apparent differences in the mode of deterioration among the three rows of outer hair cells. Stereocilia fusion of inner hair cells occurred at an older age, and giant, elongated stereocilia were found in some of the animals.

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Roberts, DG. "Root-hair structure and development in the seagrass Halophila ovalis (R. Br.) Hook. F." Marine and Freshwater Research 44, no. 1 (1993): 85. http://dx.doi.org/10.1071/mf9930085.

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The seagrass Halophila ovalis normally produces one mature root, covered with a permanent mat of root hairs, per node. In this study, the development of the root hairs increased the effective root surface absorptive area by 215%. Of the root surface examined, 39% was devoted to root-hair production. Epidermal cells that produced root hairs contained more cytoplasm, endoplasmic reticulum and Golgi bodies than did adjacent hairless cells. In addition to appearing to be more metabolically active, root-hair-producing cells had a greater number of plasmodesmatal connections with the underlying outer cortical cells than did adjacent cells that did not produce root hairs. This would suggest that cells that produce root hairs play a more active role in nutrient uptake and exchange than do other cortical cells.

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Wiwatpanit, Teerawat, Sarah M. Lorenzen, Jorge A. Cantú, Chuan Zhi Foo, Ann K. Hogan, Freddie Márquez, John C. Clancy, et al. "Trans-differentiation of outer hair cells into inner hair cells in the absence of INSM1." Nature 563, no. 7733 (October 10, 2018): 691–95. http://dx.doi.org/10.1038/s41586-018-0570-8.

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Drexl, Markus, Marcia M. Mellado Lagarde, Jian Zuo, Andrei N. Lukashkin, and Ian J. Russell. "The Role of Prestin in the Generation of Electrically Evoked Otoacoustic Emissions in Mice." Journal of Neurophysiology 99, no. 4 (April 2008): 1607–15. http://dx.doi.org/10.1152/jn.01216.2007.

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Electrically evoked otoacoustic emissions are sounds emitted from the inner ear when alternating current is injected into the cochlea. Their temporal structure consists of short- and long-delay components and they have been attributed to the motile responses of the sensory-motor outer hair cells of the cochlea. The nature of these motile responses is unresolved and may depend on either somatic motility, hair bundle motility, or both. The short-delay component persists after almost complete elimination of outer hair cells. Outer hair cells are thus not the sole generators of electrically evoked otoacoustic emissions. We used prestin knockout mice, in which the motor protein prestin is absent from the lateral walls of outer hair cells, and Tecta ΔENT/ΔENT mice, in which the tectorial membrane, a structure with which the hair bundles of outer hair cells normally interact, is vestigial and completely detached from the organ of Corti. The amplitudes and delay spectra of electrically evoked otoacoustic emissions from Tecta ΔENT/ΔENT and Tecta +/+ mice are very similar. In comparison with prestin +/+ mice, however, the short-delay component of the emission in prestin −/− mice is dramatically reduced and the long-delay component is completely absent. Emissions are completely suppressed in wild-type and Tecta ΔENT/ΔENT mice at low stimulus levels, when prestin-based motility is blocked by salicylate. We conclude that near threshold, the emissions are generated by prestin-based somatic motility.

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Nadol, Joseph B., and Aaron R. Thornton. "Ultrastructural Findings in a Case of Meniere's Disease." Annals of Otology, Rhinology & Laryngology 96, no. 4 (July 1987): 449–54. http://dx.doi.org/10.1177/000348948709600420.

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The temporal bones of an individual with documented unilateral Meniere's disease were prepared for light and electron microscopy. a morphometric analysis was performed on hair cells, spiral ganglion cells, dendritic fibers in the osseous spiral lamina, afferent and efferent endings, and afferent synaptic contacts. In the ear with Meniere's disease, we found hair cell damage, including disruption of the cuticular bodies and basalward displacement of some outer hair cells. There was no significant difference in the number of hair cells or spiral ganglion cells on the two sides. There was a significant decrease, however, in the number of afferent nerve endings and afferent synapses at the base of both inner and outer hair cells in the ear with Meniere's disease as compared to the contralateral ear.

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Koch, P. J., M. G. Mahoney, G. Cotsarelis, K. Rothenberger, R. M. Lavker, and J. R. Stanley. "Desmoglein 3 anchors telogen hair in the follicle." Journal of Cell Science 111, no. 17 (September 1, 1998): 2529–37. http://dx.doi.org/10.1242/jcs.111.17.2529.

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Little is known about the function of desmosomes in the normal structure and function of hair. Therefore, it was surprising that mice without desmoglein 3 (the autoantigen in pemphigus vulgaris) not only developed mucous membrane and skin lesions like pemphigus patients, but also developed hair loss. Analysis of this phenotype indicated that hair was normal through the first growth phase (‘follicular neogenesis’). Around day 20, however, when the hair follicles entered the resting phase of the hair growth cycle (telogen), mice with a targeted disruption of the desmoglein 3 gene (DSG3-/-) lost hair in a wave-like pattern from the head to the tail. Hair then regrew and was lost again in the same pattern with the next synchronous hair cycle. In adults, hair was lost in patches. Gentle hair pulls with adhesive tape showed that anagen (growing) hairs were firmly anchored in DSG3-/- mice, but telogen hairs came out in clumps compared to that of DSG3+/− and +/+ littermates in which telogen hairs were firmly anchored. Histology of bald skin areas in DSG3-/- mice showed cystic telogen hair follicles without hair shafts. Histology of hair follicles in early telogen, just before clinical hair loss occurred, showed loss of cell adhesion (acantholysis) between the cells surrounding the telogen club and the basal layer of the outer root sheath epithelium. Electron microscopy revealed ‘half-desmosomes’ at the plasma membranes of acantholytic cells. Similar acantholytic histology and ultrastructural findings have been previously reported in skin and mucous membrane lesions of DSG3-/- mice and pemphigus vulgaris patients. Immunoperoxidase staining with an antibody raised against mouse desmoglein 3 showed intense staining on the cell surface of keratinocytes surrounding the telogen hair club in normal mice. Similar staining was seen in human telogen hair with an anti-human desmoglein 3 antibody. Finally, a scalp biopsy from a pemphigus vulgaris patient showed empty telogen hair follicles. These data demonstrate that desmoglein 3 is not only critical for cell adhesion in the deep stratified squamous epithelium, but also for anchoring the telogen hair to the outer root sheath of the follicle and underscore the importance of desmosomes in maintaining the normal structure and function of hair.

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Rabbitt, R. D., H. E. Ayliffe, D. Christensen, K. Pamarthy, C. Durney, S. Clifford, and W. E. Brownell. "Evidence of Piezoelectric Resonance in Isolated Outer Hair Cells." Biophysical Journal 88, no. 3 (March 2005): 2257–65. http://dx.doi.org/10.1529/biophysj.104.050872.

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42

Qi, Mei-Hao, Yang Qiu, Ke-Yong Tian, Kun Liang, Hui-Min Chang, Ren-Feng Wang, Er-Fang Chen, Wei-Long Wang, Ding-Jun Zha, and Jian-Hua Qiu. "Outer hair cells isolation from postnatal Sprague–Dawley rats." World Journal of Otorhinolaryngology - Head and Neck Surgery 5, no. 1 (March 2019): 14–18. http://dx.doi.org/10.1016/j.wjorl.2018.01.001.

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Santos-Sacchi, Joseph, Min Wu, and Seiji Kakehata. "Furosemide alters nonlinear capacitance in isolated outer hair cells." Hearing Research 159, no. 1-2 (September 2001): 69–73. http://dx.doi.org/10.1016/s0378-5955(01)00321-5.

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He, David Z. Z., Jing Zheng, and Peter Dallos. "Development of acetylcholine receptors in cultured outer hair cells." Hearing Research 162, no. 1-2 (December 2001): 113–25. http://dx.doi.org/10.1016/s0378-5955(01)00376-8.

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Tabuchi, Keiji, Shigeki Tsuji, Kazuya Fujihira, Keiko Oikawa, Akira Hara, and Jun Kusakari. "Outer hair cells functionally and structurally deteriorate during reperfusion." Hearing Research 173, no. 1-2 (November 2002): 153–63. http://dx.doi.org/10.1016/s0378-5955(02)00349-0.

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Nenov, Anastas P., Charles Norris, and Richard P. Bobbin. "Outwardly rectifying currents in guinea pig outer hair cells." Hearing Research 105, no. 1-2 (March 1997): 146–58. http://dx.doi.org/10.1016/s0378-5955(96)00207-9.

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Puschner, Birgit, and Jochen Schacht. "Energy metabolism in cochlear outer hair cells in vitro." Hearing Research 114, no. 1-2 (December 1997): 102–6. http://dx.doi.org/10.1016/s0378-5955(97)00163-9.

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Alkon, D. L., R. Etcheberrigaray, and E. Rojas. "Distribution of voltage sensors in mammalian outer hair cells." Biophysical Journal 65, no. 5 (November 1993): 1755–56. http://dx.doi.org/10.1016/s0006-3495(93)81232-3.

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49

Brownell, W., C. Bader, D. Bertrand, and Y. de Ribaupierre. "Evoked mechanical responses of isolated cochlear outer hair cells." Science 227, no. 4683 (January 11, 1985): 194–96. http://dx.doi.org/10.1126/science.3966153.

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50

Ohmishi, Sumio, Mitsuyoshi Hara, and Chiyoko Inagaki. "Furosemide-sensitive Cl- channel in cochlear outer hair cells." Japanese Journal of Pharmacology 58 (1992): 267. http://dx.doi.org/10.1016/s0021-5198(19)49294-9.

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Journal articles on the topic 'Outer hair cells'

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