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1 on of release-ready synaptic vesicles in the cochlear hair cell.
2 lfactory receptor neurons and vestibular and cochlear hair cells.
3 myosin XVa mRNA and protein are expressed in cochlear hair cells.
4 rters and may explain observed properties of cochlear hair cells.
5 wth of stereocilia bundles in vestibular and cochlear hair cells.
6 constant-frequency neurons and contralateral cochlear hair cells.
7 rgans and is required for normal function of cochlear hair cells.
8 26SB), on mechano-electrical transduction in cochlear hair cells.
9 nsors, or pumps to control calcium levels in cochlear hair cells.
10 inetic range needed for electrical tuning of cochlear hair cells.
11 ganisation and has a role in the function of cochlear hair cells.
12 described the loss of afferent contacts from cochlear hair cells.
13 rophages following the selective ablation of cochlear hair cells.
14 synergistically in USH2 complex assembly in cochlear hair cells.
15 he USH2 complex at ankle links in developing cochlear hair cells.
16 oration to express cDNAs and shRNAs in mouse cochlear hair cells.
17 s, resulting in a toxic microenvironment for cochlear hair cells.
18 reocilia of teleost vestibular and mammalian cochlear hair cells.
19 the improper development or degeneration of cochlear hair cells.
20 ngth of the cochlear duct, and the number of cochlear hair cells.
21 oustic signal acquisition and propagation in cochlear hair cells.
22 erlie the late acquisition of BK currents in cochlear hair cells.
23 hat regulates synaptic vesicle exocytosis in cochlear hair cells.
24 and temporally precise neurotransmission by cochlear hair cells.
25 two shorter rows of stereocilia in mammalian cochlear hair cells.
26 tion of the hair bundle is lost in mammalian cochlear hair cells.
27 rons and mechanosensory stereocilia of mouse cochlear hair cells.
28 lly in retinal photoreceptors and developing cochlear hair cells.
29 al photoreceptors and for the development of cochlear hair cells.
30 lification of the mechanical stimulus by the cochlear hair cells.
32 everse-polarity" current was investigated in cochlear hair cells after tip-link destruction with BAPT
33 pment, but little is known about its role in cochlear hair cell and Deiter's support cell development
35 specific protease domain and is expressed in cochlear hair cells and a subset of supporting cells.
36 posure destroys synaptic connections between cochlear hair cells and auditory nerve fibers; however,
38 l ganglion neurons (SGNs) receive input from cochlear hair cells and project from the cochlea to the
39 sts of spontaneous activity are generated in cochlear hair cells and propagated along central auditor
42 Tmc2 were expressed in mouse vestibular and cochlear hair cells and that GFP-tagged TMC proteins loc
44 diversity of splice variants exist in rodent cochlear hair cells and this diversity is similar to tha
45 ring loss associated with mild damage to the cochlear hair cells and, strikingly, significant degener
46 lear duct, a decrease in the total number of cochlear hair cells, and defects in the formation of the
47 sion has been reported in photoreceptors and cochlear hair cells, and mutations in whirlin cause Ushe
48 ecific for vestibular hair cells, others for cochlear hair cells, and some are expressed just before
54 ssion was transient in early postnatal mouse cochlear hair cells but persisted in vestibular hair cel
55 e for Barhl1 in the long-term maintenance of cochlear hair cells, but not in the determination or dif
56 ediate the intrinsic frequency tuning of the cochlear hair cell by an electrical resonance mechanism.
57 assium currents were characterized in turtle cochlear hair cells by whole-cell voltage clamp during s
58 inoglycoside antibiotics are known toxins to cochlear hair cells, causing permanent hearing loss.
63 s Cx26 and Cx30 gene knockout mice show that cochlear hair cells degenerate after the onset of hearin
64 , partial pontine nucleus migration defects, cochlear hair cell degeneration, and profound hearing lo
68 egulating epithelial polarity, ion channels, cochlear hair cell development, vesicular sorting, and n
69 postnatal maturation of the mouse inner ear, cochlear hair cells display at least two types of mechan
70 However, SGNs degenerate following loss of cochlear hair cells, due at least in part to a reduction
71 associated with these mutations is caused by cochlear hair cell dysfunction, as indicated by conspicu
76 opment in the 1970s of objective measures of cochlear hair cell function (cochlear microphonics, otoa
77 iary localization of TRPML3 and investigated cochlear hair cell function in varitint-waddler (Va(J))
81 ness associated with a rapid degeneration of cochlear hair cells (HCs) but have a normal endocochlear
82 ns (SGNs) extend their neurites to innervate cochlear hair cells (HCs) with their soma aggregated int
83 eurons via the corticofugal system modulates cochlear hair cells in a highly specific way according t
84 tes both the hearing loss and destruction of cochlear hair cells in guinea pigs treated with aminogly
92 ly believed that mechanical amplification by cochlear hair cells is necessary to enhance the sensitiv
94 GPR98 and WHRN, to ankle links in developing cochlear hair cells, likely through its direct interacti
95 rin-1 protein expressed in transfected mouse cochlear hair cells localized to the bundle; however, th
96 ry brainstem responses (ABRs) and determined cochlear hair cell loss in 13-month-old 129/CD-1 mice wi
102 We identified >600 enriched transcripts in cochlear hair cells, of which 90% have not been previous
103 pendent hearing loss is not due to a loss of cochlear hair cells or spiral ganglion neurons, both of
104 for Notch-mediated lateral inhibition during cochlear hair cell patterning, we also detected abnormal
110 ids, open neural tube, and misorientation of cochlear hair cell stereociliary bundles, indicative of
111 ortant in sites such as the gamma-actin-rich cochlear hair cell stereocilium where local mm calcium c
112 -CreER activity was also detected in >50% of cochlear hair cells, suggesting that Sox2-CreER may not
113 fi1, two transcription factors implicated in cochlear hair cell survival, depends upon continued Atoh
114 2, is a critical gene for the development of cochlear hair cells, the receptor cells for hearing, but
115 n neurons communicate sound information from cochlear hair cells to auditory brainstem neurons throug
116 lion neurons (SGNs) relay acoustic code from cochlear hair cells to the brainstem, and their stimulat
118 ding neuronal firing, synaptic transmission, cochlear hair cell tuning, insulin release, and smooth m
119 lia organization in the cochlea, and rescues cochlear hair cells, vestibular function and low-frequen
120 l synapses mediate cholinergic inhibition of cochlear hair cells via alpha9alpha10-containing ionotro
121 Otoferlin, the proposed Ca(2+) sensor in cochlear hair cells, was similarly distributed in both c
123 toxicity, changes in lysosomal activities in cochlear hair cells were evaluated during a repeated adm
124 hlear function was rapidly abolished and all cochlear hair cells were missing within 24 h after treat
125 g loss accompanied by loss of mechanosensory cochlear hair cells, while the endocochlear potential an
126 rapy for patients with hereditary absence of cochlear hair cells, who have severe or profound deafnes
127 mice resulted in nearly complete ablation of cochlear hair cells, with no evident pathology among sup
128 for specific Usher protein variants in mouse cochlear hair cells, with the apical variants playing a
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