Browse
Submit Data
Databases
API
Help

Dataset Information

20 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

The role of ear stone size in hair cell acoustic sensory transduction.

ABSTRACT: Hearing and bodily balance are different sensations initiated by a common mechanism. Both sound- and head movement-dependent mechanical displacement are converted into electrical signals by the sensory hair cells. The saccule and utricle inner ear organs, in combination with their central projections to the hindbrain, are considered essential in fish for separating auditory and vestibular stimuli. Here, we established an in vivo method in larval zebrafish to manipulate otolith growth. We found that the saccule containing a large otolith is necessary to detect sound, whereas the utricle containing a small otolith is not sufficient. Otolith removal and relocation altered otolith growth such that utricles with experimentally enlarged otoliths acquired the sense of sound. These results show that otolith biomineralization occurs in a region-specific manner, and suggest that regulation of otolith size in the larval zebrafish ear is crucial to differentially sense auditory and vestibular information.

SUBMITTER: Inoue M

PROVIDER: S-EPMC3698489 | biostudies-literature | 2013

REPOSITORIES: biostudies-literature

ACCESS DATA

Json Xml

Publications

The role of ear stone size in hair cell acoustic sensory transduction.

Inoue Maya M Tanimoto Masashi M Oda Yoichi Y

Scientific reports 20130101

Hearing and bodily balance are different sensations initiated by a common mechanism. Both sound- and head movement-dependent mechanical displacement are converted into electrical signals by the sensory hair cells. The saccule and utricle inner ear organs, in combination with their central projections to the hindbrain, are considered essential in fish for separating auditory and vestibular stimuli. Here, we established an in vivo method in larval zebrafish to manipulate otolith growth. We found t ...[more]

PMID: 23817603

Similar Datasets

Developmental acquisition of sensory transduction in hair cells of the mouse inner ear.

Project description:Sensory transduction in hair cells requires assembly of membrane-bound transduction channels, extracellular tip-links and intracellular adaptation motors with sufficient precision to confer nanometer displacement sensitivity. Here we present evidence based on FM1-43 fluorescence, scanning electron microscopy and RT-PCR that these three essential elements are acquired concurrently between embryonic day 16 and 17, several days after the appearance of hair bundles, and that their acquisition coincides with the onset of mechanotransduction.

| S-EPMC2669437 | biostudies-literature

Exosomes mediate sensory hair cell protection in the inner ear.

Project description:Hair cells, the mechanosensory receptors of the inner ear, are responsible for hearing and balance. Hair cell death and consequent hearing loss are common results of treatment with ototoxic drugs, including the widely used aminoglycoside antibiotics. Induction of heat shock proteins (HSPs) confers protection against aminoglycoside-induced hair cell death via paracrine signaling that requires extracellular heat shock 70-kDa protein (HSP70). We investigated the mechanisms underlying this non-cell-autonomous protective signaling in the inner ear. In response to heat stress, inner ear tissue releases exosomes that carry HSP70 in addition to canonical exosome markers and other proteins. Isolated exosomes from heat-shocked utricles were sufficient to improve survival of hair cells exposed to the aminoglycoside antibiotic neomycin, whereas inhibition or depletion of exosomes from the extracellular environment abolished the protective effect of heat shock. Hair cell-specific expression of the known HSP70 receptor TLR4 was required for the protective effect of exosomes, and exosomal HSP70 interacted with TLR4 on hair cells. Our results indicate that exosomes are a previously undescribed mechanism of intercellular communication in the inner ear that can mediate nonautonomous hair cell survival. Exosomes may hold potential as nanocarriers for delivery of therapeutics against hearing loss.

| S-EPMC7190999 | biostudies-literature

Transduction channels' gating can control friction on vibrating hair-cell bundles in the ear.

Project description:Hearing starts when sound-evoked mechanical vibrations of the hair-cell bundle activate mechanosensitive ion channels, giving birth to an electrical signal. As for any mechanical system, friction impedes movements of the hair bundle and thus constrains the sensitivity and frequency selectivity of auditory transduction. Friction is generally thought to result mainly from viscous drag by the surrounding fluid. We demonstrate here that the opening and closing of the transduction channels produce internal frictional forces that can dominate viscous drag on the micrometer-sized hair bundle. We characterized friction by analyzing hysteresis in the force-displacement relation of single hair-cell bundles in response to periodic triangular stimuli. For bundle velocities high enough to outrun adaptation, we found that frictional forces were maximal within the narrow region of deflections that elicited significant channel gating, plummeted upon application of a channel blocker, and displayed a sublinear growth for increasing bundle velocity. At low velocity, the slope of the relation between the frictional force and velocity was nearly fivefold larger than the hydrodynamic friction coefficient that was measured when the transduction machinery was decoupled from bundle motion by severing tip links. A theoretical analysis reveals that channel friction arises from coupling the dynamics of the conformational change associated with channel gating to tip-link tension. Varying channel properties affects friction, with faster channels producing smaller friction. We propose that this intrinsic source of friction may contribute to the process that sets the hair cell's characteristic frequency of responsiveness.

| S-EPMC4034190 | biostudies-literature

Sensory transduction is required for normal development and maturation of cochlear inner hair cell synapses.

Project description:Acoustic overexposure and aging can damage auditory synapses in the inner ear by a process known as synaptopathy. These insults may also damage hair bundles and the sensory transduction apparatus in auditory hair cells. However, a connection between sensory transduction and synaptopathy has not been established. To evaluate potential contributions of sensory transduction to synapse formation and development, we assessed inner hair cell synapses in several genetic models of dysfunctional sensory transduction, including mice lacking transmembrane channel-like (Tmc) 1, Tmc2, or both, in Beethoven mice which carry a dominant Tmc1 mutation and in Spinner mice which carry a recessive mutation in transmembrane inner ear (Tmie). Our analyses reveal loss of synapses in the absence of sensory transduction and preservation of synapses in Tmc1-null mice following restoration of sensory transduction via Tmc1 gene therapy. These results provide insight into the requirement of sensory transduction for hair cell synapse development and maturation.

| S-EPMC8598158 | biostudies-literature

Balancing cell numbers during organogenesis: Six1a differentially affects neurons and sensory hair cells in the inner ear.

Project description:While genes involved in the differentiation of the mechanosensory hair cells and the neurons innervating them have been identified, genes involved in balancing their relative numbers remain unknown. Six1a plays a dual role by promoting hair cell fate while inhibiting neuronal fate in these two lineages. Genes homologous to six1a act as either transcriptional activators or repressors, depending on the partners with which they interact. By assaying the in vivo and in vitro effects of mutations in presumptive protein-protein interacting and DNA-binding domains of Six1a, we show that, in the developing zebrafish inner ear, Six1a promotes hair cell fate by acting as a transcriptional activator and inhibits neuronal fate by acting as a transcriptional repressor. We also identify several potential partners for Six1a that differ between these two lineages. The dual role of Six1a in the developing otocyst provides a mechanism for balancing the relative number of hair cells and neurons during organogenesis of the inner ear.

| S-EPMC3156292 | biostudies-literature

TMC1 Forms the Pore of Mechanosensory Transduction Channels in Vertebrate Inner Ear Hair Cells.

Project description:The proteins that form the permeation pathway of mechanosensory transduction channels in inner-ear hair cells have not been definitively identified. Genetic, anatomical, and physiological evidence support a role for transmembrane channel-like protein (TMC) 1 in hair cell sensory transduction, yet the molecular function of TMC proteins remains unclear. Here, we provide biochemical evidence suggesting TMC1 assembles as a dimer, along with structural and sequence analyses suggesting similarity to dimeric TMEM16 channels. To identify the pore region of TMC1, we used cysteine mutagenesis and expressed mutant TMC1 in hair cells of Tmc1/2-null mice. Cysteine-modification reagents rapidly and irreversibly altered permeation properties of mechanosensory transduction. We propose that TMC1 is structurally similar to TMEM16 channels and includes ten transmembrane domains with four domains, S4-S7, that line the channel pore. The data provide compelling evidence that TMC1 is a pore-forming component of sensory transduction channels in auditory and vestibular hair cells.

| S-EPMC6360533 | biostudies-literature

Inner ear hair cell proteome

Project description:The mammalian inner ear subserves auditory and vestibular sensations via highly specialized cells and proteins. We show that sensory hair cells (HCs) employ hundreds of uniquely or highly expressed proteins for processes involved in transducing mechanical inputs, stimulating sensory neurons, and maintaining structure and function of these post-mitotic cells. Our proteomic analysis of purified HCs extends the existing HC transcriptome, revealing undetected gene products and isoform-specific protein expression. Comparison with mouse and human databases of genetic auditory/vestibular impairments confirms the critical role of the HC proteome for normal inner ear function, providing a cell-specific pool of candidates for novel, important HC genes. Several proteins identified exclusively in HCs by proteomics and by immunohistochemistry map to human genetic deafness loci, potentially representing new deafness genes.

2016-05-23 | MSV000079756 | MassIVE

Two cell populations participate in clearance of damaged hair cells from the sensory epithelia of the inner ear.

Project description:The cochlea and the vestibular organs are populated by resident macrophages, but their role in inner ear maintenance and pathology is not entirely clear. Resident macrophages in other organs are responsible for phagocytosis of injured or infected cells, and it is likely that macrophages in the inner ear serve a similar role. Hair cell injury causes macrophages to accumulate within proximity of damaged regions of the inner ear, either by exiting the vasculature and entering the labyrinth or by the resident macrophages reorganizing themselves through local movement to the areas of injury. Direct evidence for macrophage engulfment of apoptotic hair cells has been observed in several conditions. Here, we review evidence for phagocytosis of damaged hair cells in the sensory epithelium by tissue macrophages in the published literature and in some new experiments that are presented here as original work. Several studies also suggest that macrophages are not the only phaogocytic cells in the inner ear, but that supporting cells of the sensory epithelium also play an important role in debris clearance. We describe the various ways in which the sensory epithelia of the inner ear are adapted to eliminate damaged and dying cells. A collaborative effort between resident and migratory macrophages as well as neighboring supporting cells results in the rapid and efficient clearance of cellular debris, even in cases where hair cell loss is rapid and complete.

| S-EPMC5544544 | biostudies-literature

The influence of NF-kappaB signal-transduction pathways on the murine inner ear by acoustic overstimulation.

Project description:Nuclear factor-kappa B (NF-kappaB) comprises a family of inducible transcription factors that serve as important regulators of the host immune and inflammatory responses. The NF-kappaB signals are activated via the canonical and/or noncanonical pathways in response to diverse stimuli. The excessive action of NF-kappaB signal-transduction pathways frequently causes self-injurious phenomena such as allergic diseases, vascular disorders, and ischemia-reperfusion neuronal damage. In the inner ear, the role of NF-kappaB has not been clarified because the activated NF-kappaB signals potentially induce both cytoprotective and cytotoxic target genes after ototoxic stimulation. In the present study, we investigated the response of NF-kappaB in both the canonical and noncanonical pathways to acoustic overstimulation (117 dB/SPL/2 hr) and followed the change of inflammatory factors (inducible nitric oxide synthase [iNOS], intracellular adhesion molecule-1 [ICAM-1], and vascular cell adhesion molecule-1 [VCAM-1]) in the cochlear lateral wall (CLW) and the rest of cochlea (RoC). By means of immunohistochemistry combined with confocal microscopy and reverse transcriptase-polymerase chain reaction techniques, we found the response of NF-kappaB family members (NF-kappa B1, 2, RelA, and RelB) at the transcription level. After the NF-kappaB signaling, the inflammatory factors were significantly increased in the CLW and the RoC. Additionally, at the protein level, the prominent expression of adhesion molecules (ICAM-1 and VCAM-1) was observed in the tissue around the capillaries in the stria vascularis. These results show that acoustic overstimulation causes the NF-kappaB signaling to overexpress the inflammatory factors in the inner ear, and the up-regulation of the adhesion molecules (ICAM-1 and VCAM-1) and iNOS potentially influence the hemodynamics and the cellular integrity in the stria vascularis.

| S-EPMC2811430 | biostudies-literature

Muscle-like nicotinic receptor accessory molecules in sensory hair cells of the inner ear.

Project description:Nothing is known about the regulation of nicotinic acetylcholine receptors (nAChRs) in hair cells of the inner ear. MuSK, rapsyn and RIC-3 are accessory molecules associated with muscle and brain nAChR function. We demonstrate that these accessory molecules are expressed in the inner ear raising the possibility of a muscle-like mechanism for clustering and assembly of nAChRs in hair cells. We focused our investigations on rapsyn and RIC-3. Rapsyn interacts with the cytoplasmic loop of nAChR alpha9 subunits but not nAChR alpha10 subunits. Although rapsyn and RIC-3 increase nAChR alpha9 expression, rapsyn plays a greater role in receptor clustering while RIC-3 is important for acetylcholine-induced calcium responses. Our data suggest that RIC-3 facilitates receptor function, while rapsyn enhances receptor clustering at the cell surface.

| S-EPMC2480618 | biostudies-literature

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data