ライフサイエンスコーパス: outer hair cell

1 t constant along the length of an individual outer hair cell.

2 loss of inner hair cell synaptic ribbons and outer hair cells.

3 Prestin is the motor protein of cochlear outer hair cells.

4 rons along the cochlear duct to contact many outer hair cells.

5 ment of voltage-dependent electromotility of outer hair cells.

6 rgan of Corti MOR was expressed in inner and outer hair cells.

7 duction currents and sensitivity in cochlear outer hair cells.

8 tory currents in apical developing inner and outer hair cells.

9 frequencies, the shift is larger in shorter outer hair cells.

10 were mostly contracted and detached from the outer hair cells.

11 stological alterations and cell apoptosis of outer hair cells.

12 aluating the function of prestin in cochlear outer hair cells.

13 arker, Endo G, translocated to the nuclei of outer hair cells.

14 lls and is augmented in inner hair cells vs. outer hair cells.

15 urs via the alpha9alpha10 nAChR complexes on outer hair cells.

16 nt in the stria vascularis and the inner and outer hair cells.

17 e shifts of electromotility were observed in outer hair cells.

18 inned by electromechanical feedback from the outer hair cells.

19 munopuncta clustered at the synaptic pole of outer hair cells.

20 hair cells and spiral ganglion cells but not outer hair cells.

21 inner hair cells, but not in Myo15(sh2/sh2) outer hair cells.

22 dependence in adult rodent IHCs and immature outer hair cells.

23 voltage-driven electromotility of mammalian outer hair cells.

24 the aged cochlea, together with some loss of outer hair cells.

25 ast, it is required only for the survival of outer hair cells.

26 fewer in number and receive input from many outer hair cells.

27 e values observed in experiments on isolated outer hair cells.

28 ural mechanics, and electrophysiology of the outer hair cells.

29 ently expanded to the entire lateral wall in outer hair cells.

30 anti-Foxo3 immunofluorescence in adult human outer hair cells.

31 potentials, drive somatic electromotility of outer hair cells.

32 to active electro-mechanical feedback of the outer hair cells.

33 ed hearing thresholds, and extensive loss of outer hair cells.

34 s in maximal vibration at the apical ends of outer hair cells.

35 l studies showed preserved cochlear receptor outer hair cell activities (otoacoustic emissions) and a

36 afferent ribbon density was reduced, whereas outer hair cell afferent ribbon density was increased.

37 restin, a terminal differentiation marker of outer hair cells, although many new hair cells eventuall

38 otoacoustic emissions, suggesting defects in outer hair cell amplification, their endocochlear potent

39 in mice with relatively little reduction in outer hair cell amplification.

40 Outer hair cells amplify and improve the frequency selec

41 Outer hair cells amplify the traveling wave within the m

42 without the push-pull action provided by the outer hair cell and Deiters cell phalangeal process.

43 co-evolved with a novel hair cell type, the outer hair cell and its constituent membrane protein, pr

44 we study a mouse model without alteration to outer hair cell and organ of Corti mechanics or to mecha

45 In summary, we suggest that these defects in outer hair cell and strial cell function are important c

46 harmacological inhibitor compound C, reduced outer hair cell and synaptic ribbon loss as well as nois

47 ntrol signals from the brainstem back to the outer hair cells and auditory-nerve fibers, respectively

48 m the reticular lamina at the apical ends of outer hair cells and from the basilar membrane using a c

49 expressed in the plasma membrane of cochlear outer hair cells and functions as a unique voltage-depen

50 ected in the entire lateral wall of cochlear outer hair cells and had an intermediary distribution (b

51 s mechanoelectrical transduction currents in outer hair cells and hence cochlear amplification is gre

52 In the mouse cochlea, Ocm is found only in outer hair cells and is localized preferentially to the

53 ostaining to quantify the MOC projections to outer hair cells and lateral OC (LOC) projections to the

54 his observation accords with the function of outer hair cells and lends support to the recent hypothe

55 elium is required for the differentiation of outer hair cells and SCs, while mesenchymal FGFRs regula

56 It appears to lack outer hair cells and some supporting cells are either ab

57 tions between ABR thresholds and the loss of outer hair cells and spiral ganglion cells, but not with

58 ormalities, there was an accelerated loss of outer hair cells and the progressive appearance of large

59 These include the cochlear outer hair cells and their singular feature, somatic ele

60 sent in Prph((-/-)) mice, demonstrating that outer hair cells and their type II afferents constitute

61 ession and current levels in Pit1(dw) mutant outer hair cells, and (3) sensory and strial cell deteri

62 ner ear and is composed of inner hair cells, outer hair cells, and highly specialized supporting cell

63 The outer hair cells are cellular actuators that are respons

64 ow that type II afferents are activated when outer hair cells are damaged.

65 Absent Foxo3, outer hair cells are lost throughout the middle and high

66 Cylindrical outer hair cells are motile and their somatic length cha

67 logically observed shapes of hair bundles of outer hair cells are near-optimal in this regard.

68 s that regulate differentiation of inner and outer hair cells are not known.

69 ne row of inner hair cells and three rows of outer hair cells are surrounded by specialized supportin

70 POAEs, suggesting a role for dopamine in the outer hair cell area.

71 ysis of the de-efferentation in inner versus outer hair cell areas suggested that outer hair cell eff

72 The ability of Anc80L65 to target outer hair cells at high rates, a requirement for restor

73 ortion product amplitude and massive loss of outer hair cells at the basal turn of the cochlea was ob

74 Among other striking features, outer hair cell bodies were extremely small and were str

75 eedback: voltage-driven contractility of the outer hair cell body and active motion of the hair bundl

76 Outer hair cells boost auditory performance in mammals.

77 tnatal days 10-13) spiral ganglion cells and outer hair cells but not inner hair cells.

78 y affects the level of mitochondrial NADH in outer hair cells, but not inner hair cells, within minut

79 ctive or destructive, which implies that the outer hair cells can either amplify or reduce vibrations

80 Our results indicate that outer hair cells can generate sufficient force to drive

81 signaling and (ii) suggest that the loss of outer hair cells causes the majority of the hearing loss

82 The lateral membrane of mammalian cochlear outer hair cells contains prestin, a protein which can a

83 instem: one pathway provides gain control on outer hair cells' contribution to cochlear amplification

84 nario where the singular organization of the outer hair cells' cortical cytoskeleton may have emerged

85 taV giant spectrin, a major component of the outer hair cells' cortical cytoskeleton.

86 differentiation is unaffected in mambo mice, outer hair cells degenerate rapidly after the first post

87 and Csb(-/-) mice lose hearing and manifest outer hair cell degeneration after systemic cisplatin tr

88 in neurons, causes profound hearing loss and outer hair cell degeneration in mice.

89 some function is preserved in low frequency outer hair cells, despite concomitant profound hearing l

90 through activation of MEKK4 is necessary for outer hair cell differentiation.

91 These results indicate that outer hair cells do not amplify the basilar membrane vib

92 The outer hair cell-driven reticular lamina vibration collab

93 versus outer hair cell areas suggested that outer hair cell efferents are the most important in mini

94 red explicitly-organ of Corti mechanics, and outer hair cell electro-mechanics.

95 active cochlear mechanics, which arises from outer hair cell electromotility and hair bundle movement

96 basilar membrane, causes a leftward shift in outer hair cell electromotility towards hyperpolarizatio

97 es may contribute to processes as diverse as outer hair cell electromotility, ion channel gating, and

98 dynamics, organ of Corti (OoC) mechanics and outer hair cell electrophysiology.

99 chanical tension, with steeper gradients for outer hair cells, emphasizing the division of labor betw

100 report restoration of function in inner and outer hair cells, enhanced hair cell survival, restorati

101 ner hair cells are of linear shape, those of outer hair cells exhibit a distinctive V-shape.

102 Surprisingly, only outer hair cells exhibit fast adaptation and sensitivity

103 Singly isolated cochlear inner and outer hair cells express HCN1 transcript, and HCN1 and H

104 ults suggest that the mechanical feedback of outer hair cells, facilitated by the organ of Corti micr

105 ti vibrates because of acoustic pressure and outer hair cell force is critical for explaining cochlea

106 riginating from acoustic pressure and active outer hair cell force to the inner hair cells that synap

107 The outer hair cell from Corti's organ possesses voltage-dep

108 rocesses resulting from the disappearance of outer hair cells from the epithelium.

109 tory brainstem response (ABR) wave 1] and in outer hair cell function [distortion product otoacoustic

110 docochlear potentials, suggesting defects in outer hair cell function and potassium recycling.

111 issions were not impaired pointing to normal outer hair cell function.

112 ted auditory thresholds combined with normal outer hair cell function.

113 tory brainstem response with preservation of outer hair cell function.

114 ith salicylate or KCl solutions that reduced outer-hair-cell function and SFOAE amplification.

115 vity at each location.SIGNIFICANCE STATEMENT Outer hair cells generate force to amplify traveling wav

116 y selectivity of mammalian hearing depend on outer hair cell-generated force, which amplifies sound-i

117 Here we demonstrate that outer hair cell-generated forces amplify traveling-wave

118 The longitudinal coupling of outer hair cell-generated forces is therefore spatially

119 The mechanical stimulation of the outer hair cell hair bundle (HB) is a key step in nonlin

120 , which is associated with the elongation of outer hair cells, has a conformation with a shorter hydr

121 pplied by the tectorial membrane (TM) on the outer hair cell HB.

122 er transducing stereocilia in both inner and outer hair cells (IHCs and OHCs).

123 t otoacoustic emissions, suggesting cochlear outer hair cell impairment.

124 of all inner hair cells and the majority of outer hair cells in an adult cochlea via virus injection

125 n highly efficient transduction of inner and outer hair cells in mice, a substantial improvement over

126 eins, is expressed predominantly by cochlear outer hair cells in subcellular regions associated with

127 efferent synapses that form later (P6-P8) on outer hair cells in the basal cochlea.

128 electron microscopy revealed degeneration of outer hair cells in the basal region of baringo, nice, a

129 Outer hair cells in the cochlea have a unique motility i

130 associated with progressive degeneration of outer hair cells in the cochlea, whereas cochlear deleti

131 tes Rho GTPase pathways, leading to death of outer hair cells in the cochlea.

132 ear positioning specifically to the death of outer hair cells in the organ of Corti and ultimately to

133 hearing loss is caused by loss or damage to outer hair cells in the organ of Corti.

134 ted by a type of sensory receptor cells (the outer hair cells) in response to the acoustic vibrations

135 ion between medial olivocochlear neurons and outer hair cells, in a two-choice visual discrimination

136 rane area and linear membrane capacitance of outer hair cells increases exponentially with the electr

137 As a result, patterns of outer hair cell innervation are coordinated with the ton

138 The outer hair cell is electromotile, its membrane motor ide

139 inner hair cells (IHCs), while expression in outer hair cells is affected tonotopically.

140 Prestin in the lateral membrane of outer hair cells, is responsible for electromotility (EM

141 h species despite normal prestin function in outer hair cells isolated from naked mole-rats.

142 dulin (Ocm), which is predominately found in outer hair cells, leads to a progressive hearing loss af

143 owed the progressive threshold elevation and outer hair cell loss characteristic of the age-related h

144 xpression correlated with ABR amplitudes and outer hair cell loss in the cochlea, but NADPHd did not.

145 uced endocochlear potential, (2) significant outer hair cell loss in the mutants, which may result fr

146 s associated with increased cochlear injury, outer hair cell loss, altered expression of cochlear met

147 Outer hair cell losses were exacerbated in the same time

148 were transfected throughout the cochlea, and outer hair cells mainly in the apex.

149 it the auditory stimulus to the brain, while outer hair cells mechanically modulate the stimulus thro

150 l5 null mutation, the unitary conductance of outer hair cell mechanotransducer (MT) channels was redu

151 provide robust mechanisms that modulate the outer hair cell-mediated active response and provide the

152 localized preferentially to the basolateral outer hair cell membrane and to the base of the hair bun

153 s of age in a basal-to-apical gradient, with outer hair cells more severely affected than inner hair

154 Our results suggest that fluid motion due to outer hair cell motility can help maintain longitudinal

155 ient of potassium ion concentration; second, outer hair cell motility causes organ of Corti deformati

156 udies found that salicylate not only affects outer hair cell motility in the cochlea, but also blocks

157 rotyrosine and Lmo4 was particularly high in outer hair cell nuclei after cisplatin treatment.

158 Outer hair cell numbers and efferent function measures (

159 However, outer hair cells of knockout mice have significantly alt

160 sduction and tip-link formation, we examined outer hair cells of mouse cochleas during development an

161 Although stereocilia of both inner and outer hair cells of Myo15(sh2/sh2) mice lack myosin-XVa

162 In both inner and outer hair cells of Myo15(sh2/sh2) mice, we found mechan

163 lion neurons provide afferent innervation to outer hair cells of the cochlea and are proposed to have

164 -4 and Sun1, another LINC complex component, outer hair cells of the cochlea form normally during dev

165 ma membranes of the stereocilia of inner and outer hair cells of the inner ear.

166 attached to the electromotile, sensorimotor outer hair cells of the organ of Corti, and that the amp

167 ochlea, with highest levels in the inner and outer hair cells of the organ of Corti, cells lining the

168 lea induce transmembrane potential along the outer hair cell (OHC) but its distribution along the cel

169 membrane-based yeast two-hybrid screen of an outer hair cell (OHC) cDNA library was performed.

170 Since inner ear outer hair cell (OHC) degeneration is a common trait of

171 Outer hair cell (OHC) electromotility enables frequency

172 in is the membrane motor protein that drives outer hair cell (OHC) electromotility, a process that is

173 Outer hair cell (OHC) electromotility, a response consis

174 f anion transporters that is responsible for outer hair cell (OHC) electromotility.

175 Outer hair cell (OHC) function was measured with the cub

176 e the discovery of otoacoustic emissions and outer hair cell (OHC) motility, the fundamental question

177 Outer hair cell (OHC) nonlinear capacitance (NLC) repres

178 The cylindrical outer hair cell (OHC) of Corti's organ drives cochlear a

179 r NO-GC2 did not influence electromechanical outer hair cell (OHC) properties, as measured by distort

180 The outer hair cell (OHC) somatic electromotility is a poten

181 providing the voltage source needed to drive outer hair cell (OHC) transducer current, which leads to

182 In the outer hair cell (OHC), the extracisternal space (ECiS) i

183 at is enhanced in amplitude and sharpness by outer hair cell (OHC)-based forces.

184 The amplifier relies on outer hair cell (OHC)-generated forces driven in part by

185 Cochlear outer hair cells (OHC) express the motor protein, presti

186 different proportions of prestin-containing outer hair cells (OHC) have on cochlear amplification.

187 Outer hair cells (OHC) possess voltage-dependent membran

188 secreted protein found in mammalian cochlear outer hair cells (OHC) that is a member of the carcinoem

189 ctrical potentials in the cochlear ducts and outer hair cells (OHC).

190 he cochlear organ of Corti, particularly the outer hair cells (OHCs) [1]; however, this epithelium is

191 Using both isolated murine outer hair cells (OHCs) and a heterologous expression sy

192 transport is investigated both in guinea-pig outer hair cells (OHCs) and in an expression system wher

193 IHCs) with various efficiencies, they infect outer hair cells (OHCs) and supporting cells at lower le

194 tion was observed around postnatal day 14 in outer hair cells (OHCs) and supporting cells surrounding

195 s type II neurons arborize extensively among outer hair cells (OHCs) and supporting cells.

196 compound C attenuated noise-induced loss of outer hair cells (OHCs) and synaptic ribbons, and preser

197 Outer hair cells (OHCs) are a mammalian innovation for m

198 Cochlear outer hair cells (OHCs) are among the fastest known biol

199 Outer hair cells (OHCs) are electromotile sensory recept

200 Outer hair cells (OHCs) are highly specialized sensory c

201 Because outer hair cells (OHCs) are the only cochlear cells affe

202 how that Np55 is expressed in stereocilia of outer hair cells (OHCs) but not inner hair cells and aff

203 hanical activity termed electromotility: its outer hair cells (OHCs) change length upon electrical st

204 n heterozygous gata3 null mice (gata3(+/-) ) outer hair cells (OHCs) differentiate normally but their

205 Outer hair cells (OHCs) drive cochlear amplification tha

206 Outer hair cells (OHCs) enhance the sensitivity and the

207 Electromotility of outer hair cells (OHCs) has been extensively studied wit

208 In contrast, cochlear outer hair cells (OHCs) have a far weaker effect on thei

209 inhibitor 5-azacytidine (5-aza) to generate outer hair cells (OHCs) in a chemically-deafened adult m

210 The effectiveness of outer hair cells (OHCs) in amplifying the motion of the

211 opy was used to examine efferent synapses of outer hair cells (OHCs) in mice with diminished or enhan

212 Outer hair cells (OHCs) in the mammalian ear exhibit ele

213 ceive glutamatergic synaptic excitation from outer hair cells (OHCs) in the rat cochlea.

214 ermore, the role of afferent transmission in outer hair cells (OHCs) is not understood.

215 s evolved, now serving as a motor protein in outer hair cells (OHCs) of the mammalian inner ear and i

216 aring relies on the mechanosensory inner and outer hair cells (OHCs) of the organ of Corti, which con

217 Outer hair cells (OHCs) power the amplification of sound

218 in mammals depends on sound amplification by outer hair cells (OHCs) presumably by their somatic moti

219 The mammalian outer hair cells (OHCs) provide a positive mechanical fe

220 Outer hair cells (OHCs) provide amplification in the mam

221 ctin/spectrin-based cortical cytoskeleton of outer hair cells (OHCs) regulate their motile responses

222 neurons, with its expression being higher in outer hair cells (OHCs) than inner hair cells.

223 This requires force generation by cochlear outer hair cells (OHCs) to amplify the basilar membrane

224 cochlea is due to active forces delivered by outer hair cells (OHCs) to the cochlear partition.

225 Active force generation by outer hair cells (OHCs) underlies amplification and freq

226 bility and conductance of the MET channel of outer hair cells (OHCs) were reduced.

227 Prestin is the motor protein of cochlear outer hair cells (OHCs) with the unique capability of pe

228 earing loss without increasing the damage to outer hair cells (OHCs), but increased synaptopathy and

229 In Baiap2l2 deficient mice, outer hair cells (OHCs), but not inner hair cells (IHCs)

230 cisplatin toxicity in the inner ear, mainly outer hair cells (OHCs), inner hair cells, stria vascula

231 nstem olivary complex project to and inhibit outer hair cells (OHCs), refining acoustic sensitivity o

232 iverge to contact inner hair cells (IHCs) or outer hair cells (OHCs), respectively.

233 The function of outer hair cells (OHCs), the mechanical actuators of the

234 c stimulation, displaces the hair bundles of outer hair cells (OHCs), thereby initiating sensory tran

235 lea depends upon specialized hair cells, the outer hair cells (OHCs), which possess both sensory and

236 the electromechanical properties of cochlear outer hair cells (OHCs).

237 ransducer cells, inner hair cells (IHCs) and outer hair cells (OHCs).

238 osted by electromechanical forces in sensory outer hair cells (OHCs).

239 mechanical amplification process mediated by outer hair cells (OHCs).

240 ndly deaf, and there was substantial loss of outer hair cells (OHCs).

241 y cells, including those associated with the outer hair cells (OHCs).

242 s along the cochlear spiral, contacting many outer hair cells (OHCs).

243 In its native cochlear outer hair cell, prestin is crucial to the amplification

244 ed high-frequency regions, where the sensory outer hair cells produce force that greatly increases th

245 LC-PK1-CL4 epithelial cells (CL4 cells), the outer hair cell protein prestin showed faithful domain-s

246 Outer hair cells provide amplification within the mammal

247 While it is generally agreed that outer hair cells provide the amplification, two mechanis

248 were initiated by local tissue damage in the outer hair cell region.

249 Myo15(sh2/sh2) outer hair cells retain a staircase arrangement of the a

250 t kilohertz rates, which is required for the outer hair cells' role as a cochlear amplifier.

251 The model also demonstrates how the outer hair cell's adaptation alters the temporal pattern

252 esponse is ascribed to the saturation of the outer hair cell's mechano-transduction.

253 viable mechanism as it is not limited by the outer hair cell's membrane time constant as previously s

254 First, the phase of the outer hair cell's somatic force with respect to its elon

255 In St3gal5(-/-) mice, stereocilia of outer hair cells showed signs of degeneration as early a

256 Prestin drives outer hair cell somatic motility and amplifies mechanica

257 educing the spread of energy provided by the outer hair cells' somatic motility.

258 ows, with one row of inner and three rows of outer hair cells spanning the length of the spiral-shape

259 ells and outer pillar cells, which constrain outer hair cells standing on the basilar membrane, cause

260 ea are attributed to amplification involving outer hair cell stereocilia and/or somatic motility.

261 found that the structures that stimulate the outer hair cell stereocilia, the tectorial membrane and

262 stereocilia and progressive degeneration of outer hair cell stereocilia.

263 reveals persistent damage to some surviving outer hair cell stereocilia.

264 stereocilia and progressive degeneration of outer hair cells stereocilia.

265 ethods, we modeled an inner hair-cell and an outer hair-cell stereocilia bundle and simulated the eff

266 iliary growth and differentiation as well as outer hair cell stereociliary rigidity and organization

267 es ago and derives from the observation that outer hair cell surface area is voltage-dependent.

268 ate Foxo3 and its transcriptional targets in outer hair cell survival after noise damage.

269 ical, stemming from active mechanisms within outer hair cells that amplify the basilar membrane trave

270 rgeted inactivation of prestin, a protein of outer hair cells that generates forces on the basilar me

271 Prestin is the membrane protein in outer hair cells that harnesses electrical energy by cha

272 omechanical transduction process in cochlear outer hair cells that increases hearing sensitivity and

273 logy revealed a significant loss of SGNs and outer hair cells that strongly correlated to the level o

274 tructure in the organ of Corti formed by the outer hair cell, the Deiters cell, and the Deiters cell

275 rs and is responsible for electromotility in outer hair cells, the basis of cochlear amplification in

276 ents have shown a much larger conductance in outer hair cells, the central components of the mammalia

277 iffer gating springs, such as those from rat outer hair cells, the channel must be tethered for all b

278 ity range, depends on mechanical coupling of outer hair cells to the tectorial membrane.

279 n product otoacoustic emissions derived from outer hair cell transduction and decreased suprathreshol

280 gests that the high-frequency cut-off of the outer hair cell transmembrane potential in vivo may be n

281 r, type II afferents are weakly activated by outer hair cell transmitter release and are insensitive

282 Tuning in mammals uses somatic motility of outer hair cells, underpinned by the membrane protein pr

283 and hair-bundle motility of the thousands of outer hair cells uniquely found in mammalian cochleae.

284 Thus, the RC corner of a short outer hair cell used for high-frequency amplification do

285 he organ of Corti complex felt by individual outer hair cells varies along the cochlear length.

286 Loss of outer hair cells was evident 1 h after noise exposure in

287 r cells were absent and by P16 all inner and outer hair cells were absent in DTR mice.

288 Physiological properties for the outer hair cells were incorporated, such as the active f

289 The cochleae outer hair cells were reduced from 5-10% at one month to

290 ti vibrations, including those of individual outer hair cells, were measured using optical coherence

291 expressed in the basal membrane of cochlear outer hair cells where it may mediate K(+) efflux.

292 II spiral ganglion neuron innervation of the outer hair cells, whereas innervation of the inner hair

293 sensitivity of mammalian hearing depends on outer hair cells which generate forces for amplifying so

294 onfers electromotility on mammalian cochlear outer hair cells, which is essential for normal hearing

295 sensitivity stems from the active process of outer hair cells, which possess two force-generating mec

296 We studied both inner and outer hair cells, which send nervous signals to the brai

297 ical to maintain a stable mechanical link of outer hair cells with the tectorial membrane.

298 de-diuretic combination produced loss of all outer hair cells within 48 hours in both strains.

299 8-positive inner hair cells and reduction of outer hair cells without affecting the overall hair cell

300 In this case, the absence of outer hair cells would be compatible with overexposure t