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1

Hoben, Richard, and Mark A. Parker. "Outer Hair Cell Damage." Hearing Journal 69, no. 6 (June 2016): 10. http://dx.doi.org/10.1097/01.hj.0000484546.98172.7a.

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2

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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3

Santos-Sacchi, J. "Harmonics of outer hair cell motility." Biophysical Journal 65, no. 5 (November 1993): 2217–27. http://dx.doi.org/10.1016/s0006-3495(93)81247-5.

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4

Lue, Allen Jung-Chen, Hong-Bo Zhao, and William E. Brownell. "Chlorpromazine Alters Outer Hair Cell Electromotility." Otolaryngology–Head and Neck Surgery 125, no. 1 (July 2001): 71–76. http://dx.doi.org/10.1067/mhn.2001.116446.

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5

Deo, Niranjan, and Karl Grosh. "Simplified nonlinear outer hair cell models." Journal of the Acoustical Society of America 117, no. 4 (April 2005): 2141–46. http://dx.doi.org/10.1121/1.1871753.

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6

Iwasa, K. H., M. Ospeck, and X. x. Dong. "S02 Physical Aspect of Outer Hair Cell motility : Outer Hair Cell Motility as Two-State Piezoelectricity." Proceedings of the Bioengineering Conference Annual Meeting of BED/JSME 2001.13 (2001): 4–5. http://dx.doi.org/10.1299/jsmebio.2001.13.4.

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7

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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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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9

Harasztosi, Csaba, Entcho Klenske, and Anthony W. Gummer. "Vesicle traffic in the outer hair cell." European Journal of Neuroscience 54, no. 3 (July 5, 2021): 4755–67. http://dx.doi.org/10.1111/ejn.15331.

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10

Srinivasan, Sridhar, Andreas Keil, Kyle Stratis, Aaron F. Osborne, Colin Cerwonka, Jennifer Wong, Brenda L. Rieger, Valerie Polcz, and David W. Smith. "Interaural attention modulates outer hair cell function." European Journal of Neuroscience 40, no. 12 (October 10, 2014): 3785–92. http://dx.doi.org/10.1111/ejn.12746.

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11

Rabbitt, Richard D. "The cochlear outer hair cell speed paradox." Proceedings of the National Academy of Sciences 117, no. 36 (August 26, 2020): 21880–88. http://dx.doi.org/10.1073/pnas.2003838117.

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Cochlear outer hair cells (OHCs) are among the fastest known biological motors and are essential for high-frequency hearing in mammals. It is commonly hypothesized that OHCs amplify vibrations in the cochlea through cycle-by-cycle changes in length, but recent data suggest OHCs are low-pass filtered and unable to follow high-frequency signals. The fact that OHCs are required for high-frequency hearing but appear to be throttled by slow electromotility is the “OHC speed paradox.” The present report resolves this paradox and reveals origins of ultrafast OHC function and power output in the context of the cochlear load. Results demonstrate that the speed of electromotility reflects how fast the cell can extend against the load, and does not reflect the intrinsic speed of the motor element itself or the nearly instantaneous speed at which the coulomb force is transmitted. OHC power output at auditory frequencies is revealed by emergence of an imaginary nonlinear capacitance reflecting the phase of electrical charge displacement required for the motor to overcome the viscous cochlear load.
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12

Slepecky, Norma B. "Outer Hair Cell Morphology Related to Function." Ear, Nose & Throat Journal 76, no. 3 (March 1997): 145–50. http://dx.doi.org/10.1177/014556139707600308.

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13

Szönyi, Magdolna, David Z. Z. He, Ottó Ribári, István Sziklai, and Peter Dallos. "Cyclic GMP and outer hair cell electromotility." Hearing Research 137, no. 1-2 (November 1999): 29–42. http://dx.doi.org/10.1016/s0378-5955(99)00127-6.

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14

Szönyi, Magdolna, David Z. Z. He, Ottó Ribári, István Sziklai, and Peter Dallos. "Intracellular calcium and outer hair cell electromotility." Brain Research 922, no. 1 (December 2001): 65–70. http://dx.doi.org/10.1016/s0006-8993(01)03150-x.

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15

Kakehata, Seiji, Peter Dallos, William E. Brownell, Kuni H. Iwasa, Bechara Kachar, Federico Kalinec, Katsuhisa Ikeda, and Tomonori Takasaka. "Current concept of outer hair cell motility." Auris Nasus Larynx 27, no. 4 (October 2000): 349–55. http://dx.doi.org/10.1016/s0385-8146(00)00081-x.

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16

Brownell, William E. "Outer Hair Cell Electromotility and Otoacoustic Emissions." Ear and Hearing 11, no. 2 (April 1990): 82–92. http://dx.doi.org/10.1097/00003446-199004000-00003.

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17

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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18

Joyce, Bryan S., and Pablo A. Tarazaga. "A study of active artificial hair cell models inspired by outer hair cell somatic motility." Journal of Intelligent Material Systems and Structures 28, no. 6 (July 28, 2016): 811–23. http://dx.doi.org/10.1177/1045389x16657425.

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The cochlea displays an important, nonlinear amplification of sound-induced oscillations. In mammals, this amplification is largely powered by the somatic motility of the outer hair cells. The resulting cochlear amplifier has three important characteristics useful for hearing: an amplification of responses from low sound pressures, an improvement in frequency selectivity, and an ability to transduce a broad range of sound pressure levels. These useful features can be incorporated into designs for active artificial hair cells, bio-inspired sensors for use as microphones, accelerometers, or other dynamic sensors. The sensor consists of a cantilever beam with piezoelectric actuators. A feedback controller applies a voltage to the actuators to mimic the outer hair cells’ somatic motility. This article describes three control laws for an active artificial hair cell inspired by models of the outer hair cells’ somatic motility. The first control law is based on a phenomenological model of the cochlea while the second and third models incorporate physiological aspects of the biological cochlea to further improve sensor performance. Simulations show that these models qualitatively reproduce the key aspects of the mammalian cochlea, namely, amplification of oscillations from weak stimuli, higher quality factors, and a wider input dynamic range.
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19

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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20

Zhu, Zenghao, Anthony J. Ricci, and Daibhid O. Maoileidigh. "The functional role of connectors in outer-hair-cell hair bundles." Biophysical Journal 121, no. 3 (February 2022): 436a. http://dx.doi.org/10.1016/j.bpj.2021.11.589.

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21

Myers, Eugene N., Melville J. da Cruz, Paul Fagan, Marcus Atlas, and Celene Mcneill. "Drill-Induced Hearing Loss in the Nonoperated Ear." Otolaryngology–Head and Neck Surgery 117, no. 5 (November 1997): 555–58. http://dx.doi.org/10.1016/s0194-59989770030-5.

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The reversible hearing loss in the nonoperated ear noted by patients after ear surgery remains unexplained. This study proposes that this hearing loss is caused by drill noise conducted to the nonoperated ear by vibrations of the intact skull. This noise exposure results in dysfunction of the outer hair cells, which may produce a temporary hearing loss. Estimations of outer hair cell function in the nonoperated ear were made by recording the change in amplitude of the distortion-product otoacoustic emissions before and during ear surgery. Reversible drill-related outer hair cell dysfunction was seen in 2 of 12 cases. The changes In outer hair cell function and their clinical implications are discussed.
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22

Jerry, Rocco A., and Ashim Dutta. "Molecular Motor and Electrokinetic Contributions to Outer Hair Cell Electromotility." Journal of Neurophysiology 79, no. 1 (January 1, 1998): 471–73. http://dx.doi.org/10.1152/jn.1998.79.1.471.

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Jerry, Rocco A. and Ashim Dutta. Molecular motor and electrokinetic contributions to outer hair cell electromotility. J. Neurophysiol. 79: 471–473, 1998. The outer hair cell of the inner ear is believed to be responsible for the high sensitivity and selectivity of mammalian hearing. Molecular motors are generally believed to cause the electrically-driven length change (electromotility) of the outer hair cell. It has been suggested that electrokinetic effects might also play a significant role in electromotility, along with the molecular motors. This paper describes a new technique that can be used to experimentally determine the percentage of the electromotile response that is caused by electrokinetic effects. The technique is based on the novel idea that molecular motor activity cannot in itself generate a net force on the cell, but that electrokinetic effects can. Our method is the first that can separate molecular motor behavior from electrokinetic behavior, during experiments on the outer hair cell.
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23

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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24

Santos-Sacchi, J. "Effect of aspirin on outer hair cell motility." AUDIOLOGY JAPAN 39, no. 5 (1996): 481–82. http://dx.doi.org/10.4295/audiology.39.481.

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25

Rabbitt, Richard D., Sarah Clifford, Kathryn D. Breneman, Brenda Farrell, and William E. Brownell. "Power Efficiency of Outer Hair Cell Somatic Electromotility." PLoS Computational Biology 5, no. 7 (July 24, 2009): e1000444. http://dx.doi.org/10.1371/journal.pcbi.1000444.

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26

Fridberger, Anders, Miriam Von Tiedemann, Åke Flock, Britta Flock, Lars-Göran Öfverstedt, and Ulf Skoglund. "Three-dimensional structure of outer hair cell pillars." Acta Oto-Laryngologica 129, no. 9 (January 2009): 940–45. http://dx.doi.org/10.1080/00016480802552519.

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27

Santos-Sacchi, J., and Guojie Huang. "Temperature dependence of outer hair cell nonlinear capacitance." Hearing Research 116, no. 1-2 (February 1998): 99–106. http://dx.doi.org/10.1016/s0378-5955(97)00204-9.

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28

Sugata, Yoshinori, and Yasuo Harada. "Electrophysiological Study on a Cochlear Outer Hair Cell." Auris Nasus Larynx 18, no. 2 (January 1991): 107–14. http://dx.doi.org/10.1016/s0385-8146(12)80214-8.

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29

Iwasa, Kuni H. "Energy Output from a Single Outer Hair Cell." Biophysical Journal 111, no. 11 (December 2016): 2500–2511. http://dx.doi.org/10.1016/j.bpj.2016.10.021.

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30

Gale, J. E., and J. F. Ashmore. "The outer hair cell motor in membrane patches." Pfl�gers Archiv European Journal of Physiology 434, no. 3 (June 16, 1997): 267–71. http://dx.doi.org/10.1007/s004240050395.

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31

Lim, David J., Yutaka Hanamure, and Yoshihiro Ohashi. "Structural Organization of the Outer Hair Cell Wall." Acta Oto-Laryngologica 107, no. 5-6 (January 1989): 398–405. http://dx.doi.org/10.3109/00016488909127529.

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32

Mountain, David C., and Allyn E. Hubbard. "A piezoelectric model of outer hair cell function." Journal of the Acoustical Society of America 95, no. 1 (January 1994): 350–54. http://dx.doi.org/10.1121/1.408273.

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33

Okayasu, Tadao, Tadashi Nishimura, Akinori Yamashita, Osamu Saito, Toshiaki Yamanaka, Hiroshi Hosoi, and Tadashi Kitahara. "Outer hair cell function in human ultrasonic perception." Journal of the Acoustical Society of America 140, no. 4 (October 2016): 3156. http://dx.doi.org/10.1121/1.4969901.

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34

Cheatham, Mary Ann, Roxanne M. Edge, Kazuaki Homma, Emily L. Leserman, Peter Dallos, and Jing Zheng. "Prestin-Dependence of Outer Hair Cell Survival and Partial Rescue of Outer Hair Cell Loss in PrestinV499G/Y501H Knockin Mice." PLOS ONE 10, no. 12 (December 18, 2015): e0145428. http://dx.doi.org/10.1371/journal.pone.0145428.

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35

Ikäheimo, Kuu, Anni Herranen, Vilma Iivanainen, Tuuli Lankinen, Antti A. Aarnisalo, Ville Sivonen, Kashyap A. Patel, et al. "MANF supports the inner hair cell synapse and the outer hair cell stereocilia bundle in the cochlea." Life Science Alliance 5, no. 2 (November 23, 2021): e202101068. http://dx.doi.org/10.26508/lsa.202101068.

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Failure in the structural maintenance of the hair cell stereocilia bundle and ribbon synapse causes hearing loss. Here, we have studied how ER stress elicits hair cell pathology, using mouse models with inactivation of Manf (mesencephalic astrocyte-derived neurotrophic factor), encoding an ER-homeostasis-promoting protein. From hearing onset, Manf deficiency caused disarray of the outer hair cell stereocilia bundle and reduced cochlear sound amplification capability throughout the tonotopic axis. In high-frequency outer hair cells, the pathology ended in molecular changes in the stereocilia taper region and in strong stereocilia fusion. In high-frequency inner hair cells, Manf deficiency degraded ribbon synapses. The altered phenotype strongly depended on the mouse genetic background. Altogether, the failure in the ER homeostasis maintenance induced early-onset stereociliopathy and synaptopathy and accelerated the effect of genetic causes driving age-related hearing loss. Correspondingly, MANF mutation in a human patient induced severe sensorineural hearing loss from a young age onward. Thus, we present MANF as a novel protein and ER stress as a mechanism that regulate auditory hair cell maintenance in both mice and humans.
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36

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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37

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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38

Chole, Richard A., and Maggie Chiu. "Cochlear Hair Cell Loss in Ears with Cholesteatomas Scanning Electron Microscopy Study." Annals of Otology, Rhinology & Laryngology 97, no. 1 (January 1988): 78–82. http://dx.doi.org/10.1177/000348948809700113.

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Cochleas from 16 Mongolian gerbils with spontaneous aural cholesteatomas, and four of similar age without cholesteatomas, were examined by scanning electron microscopy to quantify cochlear hair cell loss. Loss of hair cell stereocilia was found in all ears with cholesteatomas and was increased when compared with uninvolved ears from animals of similar age. The hair cell loss assorted with gerbilline cholesteatomas appeared to be most marked in the middle turn of the cochlea and increased in severity with increasing size of the cholesteatomas. Outer hair cells were affected more than inner hair cells. Inner and outer hair cell loss was not significantly different infected cholesteatomas versus sterile cholesteatomas. The greater damage to hair cels at the middle turn compared to the basal turn suggests that these losses may be the result of some agent acting through the cochlear wall rather than through the round window.
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39

Zeng, W. Z., N. Grillet, J. B. Dewey, A. Trouillet, J. F. Krey, P. G. Barr-Gillespie, J. S. Oghalai, and U. Muller. "Neuroplastin Isoform Np55 Is Expressed in the Stereocilia of Outer Hair Cells and Required for Normal Outer Hair Cell Function." Journal of Neuroscience 36, no. 35 (August 31, 2016): 9201–16. http://dx.doi.org/10.1523/jneurosci.0093-16.2016.

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40

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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41

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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42

Santos-Sacchi, J., and J. P. Dilger. "Whole cell currents and mechanical responses of isolated outer hair cells." Hearing Research 35, no. 2-3 (September 1988): 143–50. http://dx.doi.org/10.1016/0378-5955(88)90113-x.

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43

Sandhu, Jashan, Tamara Bidone, and Richard D. Rabbitt. "Prestin Generates Instantaneous Force in Outer Hair Cell Membranes." Biophysical Journal 120, no. 3 (February 2021): 131a. http://dx.doi.org/10.1016/j.bpj.2020.11.996.

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Oghalai, John S., Takashi Nakagawa, A. A. Patel, and William E. Brownell. "Cholesterol Partitioning Within the Outer Hair Cell Lateral Wall." Otolaryngology–Head and Neck Surgery 117, no. 2 (August 1997): P91. http://dx.doi.org/10.1016/s0194-59989780127-1.

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Dallos, Peter, and Burt N. Evans. "High-Frequency Outer Hair Cell Motility: Corrections and Addendum." Science 268, no. 5216 (June 9, 1995): 1420–21. http://dx.doi.org/10.1126/science.268.5216.1420.b.

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Moglie, Marcelo J., Diego L. Wengier, A. Belén Elgoyhen, and Juan D. Goutman. "Synaptic Contributions to Cochlear Outer Hair Cell Ca2+ Dynamics." Journal of Neuroscience 41, no. 32 (July 12, 2021): 6812–21. http://dx.doi.org/10.1523/jneurosci.3008-20.2021.

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Spector, Alexander A., William E. Brownell, and Aleksander S. Popel. "Elastic Properties of the Composite Outer Hair Cell Wall." Annals of Biomedical Engineering 26, no. 1 (January 1998): 157–65. http://dx.doi.org/10.1114/1.87.

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Brownell, W. E., A. A. Spector, R. M. Raphael, and A. S. Popel. "Micro- and Nanomechanics of the Cochlear Outer Hair Cell." Annual Review of Biomedical Engineering 3, no. 1 (August 2001): 169–94. http://dx.doi.org/10.1146/annurev.bioeng.3.1.169.

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Santi, Peter A., and Vladimir L. Tsuprun. "Outer hair cell stereocilia attachment to the tectorial membrane." Journal of the Acoustical Society of America 100, no. 4 (October 1996): 2629–30. http://dx.doi.org/10.1121/1.417735.

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Frolenkov, Gregory I. "Regulation of electromotility in the cochlear outer hair cell." Journal of Physiology 576, no. 1 (September 22, 2006): 43–48. http://dx.doi.org/10.1113/jphysiol.2006.114975.

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