ライフサイエンスコーパス: vestibular

1 Of 109 cranial schwannomas, 106 (97.2%) were vestibular.

2 ely 30%, suggesting that both hair cells and vestibular afferent fibers are normally recruited by GVS

3 etylcholine receptors (nAChRs) in regulating vestibular afferent gain and activation timing.

4 by applying temporally precise activation of vestibular afferents in awake-behaving monkeys to link p

5 me that efferent-mediated slow excitation of vestibular afferents is mediated by muscarinic acetylcho

6 Efferent-mediated slow excitation of vestibular afferents is of considerable interest given i

7 ing from neurons receiving direct input from vestibular afferents within minutes, as well as a decrea

8 keys during temporally precise activation of vestibular afferents.

9 However, some auditory, vestibular and cerebellar synapses maintain constant str

10 ee compartments of the mouse inner ear - the vestibular and cochlear sensory epithelia and the spiral

11 nctional brain imaging [8], and treatment of vestibular and higher-level attentional disorders by int

12 ternal model can combine motor commands with vestibular and proprioceptive signals optimally.

13 functionally distinct components: the dorsal vestibular and ventral auditory compartments.

14 Previous research described both visuo-vestibular and vestibular-tactile bilateral interactions

15 ipants' sensory organisation (somatosensory, vestibular and visual ratios), balance and motor profici

16 uli into electrical signals in the auditory, vestibular, and lateral-line systems of vertebrates.

17 display impairment of the visual, auditory, vestibular, and olfactory systems, attributable to profo

18 Progress in biomedical technology (cochlear, vestibular, and retinal implants) has led to remarkable

19 odel for nonsyndromic deafness with enlarged vestibular aqueduct (EVA; OMIM #600791).

20 esponsible for hearing loss with an enlarged vestibular aqueduct and Pendred syndrome.

21 At least two vestibular areas are located at this site: the parietoin

22 oved vestibular function; however, no direct vestibular assessment was made.

23 cells seen in previous studies that damaged vestibular-associated areas.

24 cdh15a transgene-mediated rescue of auditory/vestibular behavior and hair cell morphology and activit

25 RT, while no crosslinking is observed at the vestibular-binding site.

26 iating from its binding site and support our vestibular Ca(2+) sensor-model further.

27 The efferent boutons on vestibular cells in alpha9, alpha10, and alpha9/10 KOs a

28 as well as at discrete midbrain auditory and vestibular centers.

29 Cs) of the dorsal cochlear nucleus (DCN) and vestibular cerebellar cortex receive glutamatergic mossy

30 BMP signaling is required to form the vestibular compartment, but how it complements other req

31 d in the literature to be a key parameter of vestibular compensation.

32 ative to a muscle's action, we show that the vestibular contribution to muscle activity is a highly f

33 Our results demonstrate that vestibular control of the upper limb maintains reaching

34 fixed task, demonstrating task dependency in vestibular control of the upper limb.

35 are located at this site: the parietoinsular vestibular cortex (PIVC) and the posterior insular corte

36 dial superior temporal area, parieto-insular vestibular cortex (PIVC), areas V6 and V6A, and cingulat

37 n has a cross-modal modulatory effect on the vestibular cortex during visual object tracking.

38 We find that activity in the parietoinsular vestibular cortex is more strongly suppressed the greate

39 effect of attention on the activation in the vestibular cortex, despite constant visual motion stimul

40 e cross-modal attention effects in the human vestibular cortex.

41 st cross-modal attentional modulation in the vestibular cortex.

42 ning that persists in virtual reality, where vestibular cues are absent.

43 derpins somatosensory modulation: visual and vestibular cues are first combined to produce a multisen

44 ns in the dark implies a privileged role for vestibular cues during human angular orientation.

45 estibular percept, and not by the visual and vestibular cues independently.

46 rtex (RSC) and thalamus, code for visual and vestibular cues of orientation, respectively.

47 macaque area MSTd that integrate visual and vestibular cues regarding self-motion.

48 o dissociate the contributions of visual and vestibular cues, we made similar measurements in virtual

49 ain is central to the cortical processing of vestibular cues.

50 al expression of Dlx5 and Hmx3 during dorsal vestibular development.

51 BACKGROUND/AIMS: Patients with vestibular disease have been observed to have concomitan

52 department with a diagnosis of a peripheral vestibular disorder was extremely low.

53 t who were given a diagnosis of a peripheral vestibular disorder.

54 11, with a primary diagnosis of a peripheral vestibular disorder.

55 Vestibular disorders are difficult to diagnose early due

56 s for efficient gene therapy of cochlear and vestibular disorders by showing that even severe dysmorp

57 trokes, are being misdiagnosed as peripheral vestibular disorders.

58 stabilize the body along the direction of a vestibular disturbance.

59 balance response organized to compensate for vestibular disturbances.

60 t prove useful in ameliorating some forms of vestibular dysfunction by modifying ongoing primary vest

61 ty-related symptoms; and (3) the severity of vestibular dysfunction can predict whether hyperactivity

62 the severity rather than the age of onset of vestibular dysfunction differentiates whether hyperactiv

63 ids have been used to treat hearing loss and vestibular dysfunction for many years.

64 2a2 mutations cause hyperactivity; (2) it is vestibular dysfunction, which frequently co-occurs with

65 tial for using antisense technology to treat vestibular dysfunction.

66 sociated with profound retinal, auditory and vestibular dysfunction.

67 teromeric nAChR is an important component of vestibular efferent activity, other peripheral or centra

68 Stimulation of vestibular efferent neurons excites calyx and dimorphic

69 s have described the postsynaptic actions of vestibular efferent stimulation in several species, char

70 lus onset, a distinct aspect of auditory and vestibular encoding.

71 invokes a Lorentz force mechanism acting on vestibular endolymph that acts to stimulate semicircular

72 barrier (BLB) was investigated in the human vestibular endorgan, the utricular macula, using postmor

73 and humans and the more global activation of vestibular endorgans by the latter approach, this method

74 lated currents to evoke neuronal activity in vestibular endorgans in the absence of head motion.

75 s are the sensory receptors of the mammalian vestibular epithelia.

76 orrect patterning of HCs in the cochlear and vestibular epithelium.

77 limited to move in a single plane while the vestibular error direction was manipulated by having sub

78 tibular stimulus that evoked a craniocentric vestibular error of head roll.

79 oked muscle responses were greatest when the vestibular error was aligned with the balance direction

80 estibular sensory feedback, the direction of vestibular-evoked ankle compensatory responses was also

81 ence frame confirms the functional nature of vestibular-evoked arm movement.

82 The results suggest that the function of vestibular-evoked arm movements is to maintain the accur

83 efore the upper limb plays an active role in vestibular-evoked balance responses.

84 stabilize the body along the direction of a vestibular-evoked disturbance.

85 These results indicate that vestibular-evoked muscle activity is a highly flexible b

86 This velocity-dependent modulation of vestibular-evoked muscle activity was retained during sp

87 Furthermore, modulation of vestibular-evoked muscle responses occurred rapidly ( ap

88 Vestibular-evoked muscle responses were greatest when th

89 Vestibular excitatory inputs in Group I motoneurons are

90 ability of patients with complete peripheral vestibular failure to update their angular travelled dis

91 h encode transcription factors essential for vestibular formation.

92 iere's disease, reduces vertigo, but damages vestibular function and can worsen hearing.

93 ividuals with documented normal auditory and vestibular function and surgical specimens from patients

94 ence of an effective treatment of peripheral vestibular function in a mouse model of USH1C and reveal

95 These findings suggest a need to evaluate vestibular function in hearing impaired individuals, esp

96 evoked potentials (VsEPs) to directly assess vestibular function in Usher mice.

97 alleviate the vestibular symptoms and favor vestibular function recovery.

98 Importantly, vestibular function remains intact in heterozygotes up t

99 icated by sensory cell function, hearing and vestibular function, and immunologic parameters.

100 ing Atoh1-Cre, which eliminated auditory and vestibular function.

101 t at P15 was minimally effective at rescuing vestibular function.

102 l in Usher mice, indicating profound loss of vestibular function.

103 The findings were suggestive of improved vestibular function; however, no direct vestibular asses

104 ASO-29 treatment at P15 despite the profound vestibular functional deficits that persist with treatme

105 ived neurotrophic factor (BDNF) can modulate vestibular functional recovery and neurogenesis in mamma

106 served reactive neurogenesis and accelerates vestibular functional recovery.

107 usion of BDNF accelerated the restoration of vestibular functions and significantly increased UVN-ind

108 ed and prevented the complete restoration of vestibular functions.

109 of retinal ganglion cells (RGC), spiral and vestibular ganglia, inner ear and vestibular hair cell n

110 rting cells, along with close to half of the vestibular ganglion cells.

111 otion duration and travelled distance during vestibular-guided navigation.

112 nt membrane-associated protein of ~P23 mouse vestibular hair bundles, the inner ear's sensory organel

113 Auditory and vestibular hair cell bundles exhibit active mechanical o

114 spiral and vestibular ganglia, inner ear and vestibular hair cell neurons in the vestibuloacoustic sy

115 used dual patch-clamp recordings from turtle vestibular hair cells and their afferent neurons to show

116 Both type I and type ll vestibular hair cells express the alpha9 and alpha10 sub

117 and ultrastructure of efferent terminals on vestibular hair cells in alpha9, alpha10, and alpha9/10

118 Vestibular hair cells in the inner ear encode head movem

119 monly associated with damage to cochlear and vestibular hair cells or neurons.

120 ethods to demonstrate that utricular type II vestibular hair cells undergo turnover in adult mice und

121 -rich stereocilia elongation in auditory and vestibular hair cells, causing deafness and balance defe

122 s, a robust model for mammalian auditory and vestibular hair cells, we identified a urea-thiophene ca

123 oad punctate cytoplasmic distribution in the vestibular hair cells, whereas it was detected in the en

124 nner hair cells, spiral ganglion neurons and vestibular hair cells.

125 ssion, reminiscent of two subtypes of native vestibular hair cells.

126 cholinergic efferents innervating peripheral vestibular hair cells.

127 cholinergic efferents innervating peripheral vestibular hair cells.

128 cant reduction in the number of cochlear and vestibular HCs, suggesting that MEKK4 activity is essent

129 heading in neurons with congruent visual and vestibular heading preferences, whereas they stabilize t

130 In contrast, we found almost no evidence for vestibular heading signals in V6, indicating that V6 is

131 ance uses a combination of somatosensory and vestibular (i.e., inertial) cues.

132 Our findings indicate that vestibular impairment is associated with increased risk

133 e in the amplitude of the OKR in response to vestibular impairment, is diminished by silencing visual

134 ouse and human databases of genetic auditory/vestibular impairments confirms the critical role of the

135 organs in the inner ear helps to dissociate vestibular impairments that cause vertigo and imbalance

136 hat the nervous system rapidly modulates the vestibular influence of each limb separately through pro

137 f vestibular pathologies; for studies on the vestibular influence of gaze, posture, and locomotion; a

138 These results suggest that vestibular influence on ankle muscle control is adjusted

139 These results demonstrate that the vestibular influence on ankle muscles during locomotion

140 KEY POINTS: The vestibular influence on human walking is phase-dependent

141 Using a split-belt treadmill, we show that vestibular influence on locomotor activity is modulated

142 ABSTRACT: During walking, the vestibular influence on locomotor activity is phase-depe

143 Vestibular information about self-motion is combined wit

144 ndicates that the lobes integrate visual and vestibular information and control the vestibulo-ocular

145 ors responsible for transducing auditory and vestibular information into electrical signals, which ar

146 Previous studies have shown that vestibular information is critical for generating the HD

147 These findings help us understand how vestibular information is used to accommodate the variab

148 tional modulation despite the severe loss of vestibular information, challenging prevailing theories

149 bules that regulate eye movement and process vestibular information.

150 ork and are thought to be possible relays of vestibular information.

151 Furthermore, glycinergic ipsilateral vestibular inhibitory inputs are activated during the ho

152 lerates functional recovery after unilateral vestibular injury.

153 ons provide medial rectus motoneurons with a vestibular input comprising mainly head velocity.

154 INTS: Reaching movements can be perturbed by vestibular input, but the function of this response is u

155 Reaching movements can be perturbed by vestibular input, but the function of this response is u

156 during rotation to isolate the influence of vestibular input, uncontaminated by inertial factors.

157 lar dysfunction by modifying ongoing primary vestibular input.

158 nje cell learning at arbitrary phases of the vestibular input.

159 Loss of vestibular inputs may lead to impairment of these cognit

160 ich generate intrinsic mossy fibers relaying vestibular inputs to the cerebellar cortex.

161 We found that, contrarily to peripheral vestibular inputs, most Purkinje cells exhibited a mixed

162 Here we exploit a previously reported visuo-vestibular integration to investigate multisensory effec

163 ces a sustained nystagmus similar to natural vestibular lesions [5, 6].

164 Vestibular loss triggers transient increases in postsyna

165 apillaries constituting the BLB in the human vestibular macula utricle from normal and Meniere's dise

166 The independent vestibular modulation of muscle activity from each limb

167 that the cerebral cortical regions mediating vestibular-motion ('am I moving?') and vestibular-spatia

168 what brain areas are involved in converting vestibular-motion signals to those that enable such vest

169 Conversely, the vestibular mutant SERT-G402H merely displayed the high f

170 Behaviorally relevant patterns of vestibular nerve activation generated a rapid and substa

171 cat vestibular nuclei (VN) after unilateral vestibular neurectomy (UVN) and has been reported to fac

172 rain-derived neurotrophic factor potentiates vestibular neurogenesis and significantly accelerates fu

173 dition to projecting to motoneurons, central vestibular neurons also receive direct sensory input fro

174 a genetically defined population of central vestibular neurons in rhombomeres 5-7 of larval zebrafis

175 elative sparing of the efferent auditory and vestibular neurons suggests that alternate glycosphingol

176 e medial longitudinal fascicle (MLF) and the vestibular neurons through the ascending tract of Deiter

177 Finally, we found that central vestibular neurons were necessary for a vital behavior r

178 ed differentially projecting sets of central vestibular neurons.

179 ischarge rate and sensitivity of first-order vestibular neurons.

180 cell proliferation occurs rapidly in the cat vestibular nuclei (VN) after unilateral vestibular neure

181 tors, undergo remarkable fluctuations within vestibular nuclei (VN), strongly suggesting that GABA ac

182 ame millisecond time scale within inhibitory vestibular nuclei networks contributes to ensuring a rel

183 rtical structures such as the cerebellum and vestibular nuclei, cortical lesions have suggested that

184 l, comprising both the cerebellar cortex and vestibular nuclei, reproduces behavioral data and accoun

185 tentiation, and reductions in BK currents in vestibular nucleus neurons.

186 ed from those from the native ear within the vestibular nucleus, resembling the ocular dominance colu

187 r and middle reticular nuclei, magnocellular vestibular nucleus, solitary tract nucleus, nucleus medi

188 fasciculus (MLF), and neurons in the lateral vestibular nucleus, whose axons project through the asce

189 tion with optic flow, creating either purely vestibular or visuo-vestibular sensations of self-motion

190 In both the organ of Corti and the vestibular organ, impaired terminal differentiation mani

191 rowth and cellular proliferation in a murine vestibular organ, the utricle.

192 offset force-a behavior that is useful in a vestibular organ.

193 tanding of sensorineural plasticity in adult vestibular organs and further elucidate the roles that s

194 f eye movements by electrical stimulation of vestibular organs in the inner ear helps to dissociate v

195 In sensory hair cells of auditory and vestibular organs, the ribbon synapse is required for th

196 No whirlin is detected in Dfnb31(wi/wi) vestibular organs, while only C-whirlin is expressed in

197 oids that morphologically resemble inner ear vestibular organs.

198 ly C-whirlin is expressed in Dfnb31(neo/neo) vestibular organs.

199 Herein, we investigated PCP of the mouse vestibular organs.

200 uld represent novel treatment strategies for vestibular pathologies.

201 is typically used for a characterization of vestibular pathologies; for studies on the vestibular in

202 ontext of parallel work focused on how early vestibular pathways encode self-motion.

203 self-motion, as provided by a combined visuo-vestibular percept, and not by the visual and vestibular

204 fy reliable efferent neuronal markers in the vestibular periphery of turtle, to use these markers to

205 s may also target synaptic mechanisms in the vestibular periphery, and that KCNQ channel modulators m

206 del of DFNB63, we show that the auditory and vestibular phenotypes are due to a lack of mechanotransd

207 which responses are decoded according to the vestibular preferences of multisensory neurons.

208 DC formation of the visual system may act on vestibular projection refinements.

209 nner ear function, causes hyperactivity; (2) vestibular rather than auditory failure causes hyperacti

210 ment at P1, P5 or P15 resulted in sufficient vestibular recovery to support normal balance behaviors,

211 elf-motion triggers complementary visual and vestibular reflexes supporting image-stabilization and b

212 ing ASO-29 treatment have normal or elevated vestibular response thresholds when treated during a cri

213 Vestibular schwannoma (VS) is an intracranial tumor that

214 Vestibular schwannoma (VS) is the most common tumor of t

215 Vestibular schwannomas (VSs) are the most common tumours

216 position syndrome characterized by bilateral vestibular schwannomas (VSs) resulting in deafness and b

217 ial schwannoma had an LZTR1 mutation (3 were vestibular schwannomas and 1 was a nonvestibular schwann

218 redict the degree of tumor-brain adhesion of vestibular schwannomas and may provide a method to impro

219 w-grade tumors affecting the cranial nerves (vestibular schwannomas), meninges (meningiomas), and spi

220 haracterized by the development of bilateral vestibular schwannomas.

221 Vestibular segregation suggests that mechanisms comparab

222 , creating either purely vestibular or visuo-vestibular sensations of self-motion.

223 malian inner ear (IE) subserves auditory and vestibular sensations via highly specialized cells and p

224 ne therapy applications in both cochlear and vestibular sense organs.

225 ne delivery systems that target auditory and vestibular sensory cells with high efficiency, we delive

226 In the vestibular sensory epithelia, the virus transduced large

227 We measured vestibular sensory evoked potentials (VsEPs) in alpha9 k

228 Here, we measured vestibular sensory evoked potentials (VsEPs) to directly

229 ween balancing motor commands and associated vestibular sensory feedback, the direction of vestibular

230 and the result shows promising results that vestibular sensory input while walking could be affected

231 f the endosseous labyrinth, which houses the vestibular sensory organ of balance and orientation [4].

232 Notably, vestibular sensory organs of the inner ear, the maculae,

233 cally revealed the cellular substrate at the vestibular sensory periphery that is activated by electr

234 ickly reassociates new relationships between vestibular sensory signals and motor commands related to

235 monstrate that the nervous system transforms vestibular sensory signals of head motion according to a

236 By manipulating the direction of the imposed vestibular signal relative to a muscle's action, we show

237 t with both effects being driven by a common vestibular signal.

238 resentations of space, their congruence with vestibular signaling remains unclear.

239 During standing balance, vestibular signals encode head movement and are transfor

240 Thus, vestibular signals enhance the separability of joint tun

241 tion decoding, we tested the hypothesis that vestibular signals help to dissociate self-motion and ob

242 th single neuron and population levels, that vestibular signals help to dissociate self-motion and ob

243 As vestibular signals only provide inertial cues of self-mo

244 Our results thus demonstrate that vestibular signals play a critical role in dissociating

245 Behavioral studies suggest that vestibular signals play a role in dissociating object mo

246 We show that vestibular signals stabilize tuning for heading in neuro

247 transformation process from head-referenced vestibular signals to Earth-referenced body motion.

248 bodily signals (e.g., somatosensory, visual, vestibular signals), a notion referred to as bodily self

249 lar-motion signals to those that enable such vestibular-spatial orientation.

250 ating vestibular-motion ('am I moving?') and vestibular-spatial perception ('where am I?') are distin

251 ectroporation prevented normal elongation of vestibular stereocilia and irregularly widened them.

252 d C-whirlin isoforms are required for normal vestibular stereociliary growth, although they may play

253 and holding an earth-fixed object, galvanic vestibular stimulation (GVS) can evoke upper limb respon

254 Galvanic vestibular stimulation (GVS) uses modulated currents to

255 Galvanic vestibular stimulation (GVS) was used to evoke balance r

256 ation was elicited with magneto-hydrodynamic vestibular stimulation (MVS) by placing normal humans in

257 ith the Lorentz force hypothesis of magnetic vestibular stimulation and furthermore demonstrate the o

258 ABSTRACT: Vestibular stimulation can evoke responses in the arm wh

259 ring the fixed-in-space conditions, galvanic vestibular stimulation caused large changes in arm traje

260 Here, we applied galvanic vestibular stimulation concurrently with real body movem

261 Galvanic vestibular stimulation is used frequently in clinical pr

262 During the earth-fixed task, galvanic vestibular stimulation produced large polarity-dependent

263 Observations of arm movements evoked by vestibular stimulation provide some support for this mec

264 Galvanic vestibular stimulation responses were absent during the

265 Galvanic vestibular stimulation was applied concurrently during r

266 ir velocity was altered without any galvanic vestibular stimulation, indicating a compensatory arm re

267 sting rates and activation thresholds during vestibular stimulation.

268 based on its ability to associate light with vestibular stimulation.

269 tanding while being exposed to an electrical vestibular stimulus that evoked a craniocentric vestibul

270 t 0.8 m s(-1) while exposed to an electrical vestibular stimulus.

271 thickening and edematous changes within the vestibular stroma.

272 t of therapeutic approaches to alleviate the vestibular symptoms and favor vestibular function recove

273 In Syt7-knockout mice, Purkinje cell and vestibular synapses exhibit conventional use-dependent d

274 kinje cells to deep cerebellar nuclei and at vestibular synapses in mice.

275 We find that at Purkinje cell and vestibular synapses, Syt7 supports facilitation that is

276 IGNIFICANCE STATEMENT Targeting the efferent vestibular system (EVS) pharmacologically might prove us

277 nt sensory inputs including signals from the vestibular system about ongoing head movements (vestibul

278 ced could guide a more reliable screening of vestibular system deterioration.

279 suggest that asymmetric connectivity in the vestibular system facilitates representation of ethologi

280 The vestibular system is anatomically connected with widespr

281 The vestibular system of the inner ear detects head position

282 ross-modal attention effects also target the vestibular system.

283 in the cochlea and six months of age in the vestibular system.

284 rtigo, believed to be via stimulation of the vestibular system.

285 Although retinal and vestibular systems both encode translatory and rotatory

286 as the calyceal endings in the auditory and vestibular systems.

287 nd no evidence for GABA inside the visual or vestibular systems.

288 as the calyceal endings in the auditory and vestibular systems.

289 research described both visuo-vestibular and vestibular-tactile bilateral interactions, but the simul

290 expression did not parallel the established vestibular-then-auditory sequence.

291 also much higher in cochlear tissue than in vestibular tissue.

292 KEY POINTS: Vestibular type I and type II hair cells and their affer

293 iophysical properties of IK,L in adult mouse vestibular type I hair cells.

294 Individuals with vestibular vertigo also had a threefold increased odds o

295 We observed an 8.4% 1-year prevalence of vestibular vertigo among US adults.

296 In adjusted analyses, individuals with vestibular vertigo had an eightfold increased odds of 's

297 We evaluated the association between vestibular vertigo, cognitive impairment (memory loss, d

298 We evaluated the association between vestibular vertigo, cognitive impairment and psychiatric

299 sequela, including seizures (8.3%), auditory-vestibular-visual deficits (6%), focal neurologic dysfun

300 es (HR, 10.0; 95% CI, 7.0 to 15.3); auditory-vestibular-visual sensory deficits (HR, 2.3; 95% CI, 1.3