Increasing intracellular free calcium induces circumferential contractions in isolated cochlear outer hair cells

Dulon, Didier; Zajic, Gary; Schacht, Jochen

doi:10.1523/jneurosci.10-04-01388.1990

Cited by 156 publications

(109 citation statements)

References 34 publications

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“…Ionomycin at this concentration had no effects on hair-cell survival or morphology, suggesting that the concentration of Ca 2ϩ did not rise to an extreme level. Consistent with that conclusion, similar conditions raise intracellular Ca 2ϩ to only 1-2 M in cochlear hair cells (18).…”

Section: Resultssupporting

confidence: 80%

Regeneration of broken tip links and restoration of mechanical transduction in hair cells

Zhao

Yamoah

Gillespie

1996

Proc. Natl. Acad. Sci. U.S.A.

207

196

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A hair cell's tip links are thought to gate mechanoelectrical transduction channels. The susceptibility of tip links to acoustic trauma raises questions as to whether these fragile structures can be regenerated. We broke tip links with the calcium chelator 1,2-bis(O-aminophenoxy)ethane-N,N,N,N-tetraacetic acid and found that they can regenerate, albeit imperfectly, over several hours. The time course of tip-link regeneration suggests that this process may underlie recovery from temporary threshold shifts induced by noise exposure. Cycloheximide does not block tip-link regeneration, indicating that new protein synthesis is not required. The calcium ionophore ionomycin prevents regeneration, suggesting regeneration normally may be stimulated by the reduction in stereociliary Ca 2؉ when gating springs rupture and transduction channels close. Supporting the equivalence of tip links with gating springs, mechanoelectrical transduction returns over the same time period as tip links; strikingly, adaptation is substantially reduced, even 24 hr after breaking tip links.Hair cells transduce displacements of their mechanically sensitive hair bundles into electrical signals (1, 2). A hair bundle consists of about 100 stereocilia, each of which contains hundreds of crosslinked actin filaments enshrouded by plasma membrane. Stereocilia are arrayed in rows of increasing height, producing a bundle that exhibits mirror symmetry along a central axis; this axis also corresponds to the bundle's axis of highest displacement sensitivity. When a bundle is displaced along this axis, the tip of each shorter stereocilium slides along the side of its tallest neighbor. Such displacements stretch elastic mechanical elements called gating springs, which open transduction channels (3). Optimally poised to be gating springs, tip links are 5 ϫ 150 nm extracellular filaments that stretch from the tip of a stereocilium to the side of its neighbor, parallel to the plane of mirror symmetry (4). Bundle displacements that stretch tip links also open transduction channels, and displacements that slacken tip links permit channels to close. Because 1,2-bis(O-aminophenoxy)ethane-N,N,NЈ,NЈ-tetraacetic acid (BAPTA) eradicates tip links, simultaneously disrupting transduction by disengaging gating springs, tip links are thought to either be gating springs themselves or connect in series with the gating spring (5).A hair cell's transduction apparatus survives constant stimulation and occasionally experiences stimuli that can break tip links (6). If tip links indeed play an essential role in transduction, broken tip links should be replaced to maintain sensitivity to mechanical displacements. We intentionally broke tip links with BAPTA and found that they regenerate over a period of several hours. Regeneration is imperfect, as many links arise that connect stereociliary pairs not oriented along the plane of mirror symmetry. Although restoration of tip links does not require new protein synthesis, elevation of intracellular Ca 2ϩ levels effectively prev...

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Section: Resultssupporting

confidence: 80%

Regeneration of broken tip links and restoration of mechanical transduction in hair cells

Zhao

Yamoah

Gillespie

1996

Proc. Natl. Acad. Sci. U.S.A.

207

196

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“…In its role in efferent transmission, Ca 2ϩ enters through neuronal nicotinic ACh receptors to activate Ca 2ϩ -activated K ϩ channels, but the Ca 2ϩ signal will be primarily limited to the space between the cisternae and the plasma membrane. A third but incompletely understood role of Ca 2ϩ in outer hair cells is in regulating somatic electromotility (Dulon et al, 1990;Frolenkov et al, 2000;Beurg et al, 2001), which has been proposed as a mechanism for the slow efferent effects (Dallos et al, 1997;Sridhar et al, 1997). Is it possible there are large cytoplasmic transients in Ca 2ϩ produced by Ca 2ϩ -induced Ca 2ϩ release from the subsurface cisternae reminiscent of the sarcoplasmic reticulum in muscle (Saito 1983;Bannister et al, 1988)?…”

Section: Discussionmentioning

confidence: 99%

“…If Ca 2ϩ is mainly associated with control of motility, possibly a slow version (Dulon et al, 1990), neither the release mechanism nor mode of action of the divalent is properly understood. Nevertheless, it can be speculated that the large amount of endogenous calcium buffer will accelerate Ca 2ϩ transients, as it does in skeletal muscle, and also shield the subcellular organelles from large excursions in intracellular Ca 2ϩ occurring near the plasma membrane.…”

Section: Discussionmentioning

confidence: 99%

“…Primary information is conducted via the inner hair cells and their synapses onto the auditory nerve afferents, whereas outer hair cells act in parallel to boost the stimulus by electromechanical amplification (Dallos, 1992). Several facets of transduction involve intracellular calcium, including adaptation of mechanotransducer channels (Fettiplace and Ricci, 2003), afferent synaptic transmission (Brandt et al, 2003;Fuchs et al, 2003), and outer hair cell contractility (Dulon et al, 1990;Dallos et al, 1997;Frolenkov et al, 2000). The central role of calcium is underscored by the hearing loss resulting from mutations in the plasma membrane CaATPase (Kozel et al, 1998;Street et al, 1998), the extrusion path that maintains the ion at a low cytoplasmic concentration (Tucker and Fettiplace, 1995;Yamoah et al, 1998).…”

Section: Introductionmentioning

confidence: 99%

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The Concentrations of Calcium Buffering Proteins in Mammalian Cochlear Hair Cells

Hackney¹,

Mahendrasingam²,

Penn³

et al. 2005

J. Neurosci.

189

184

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“…Patuzzi (2011) suggested that the Bounce is due to oscillations in outer hair cell (OHC) Ca 2+ levels as a result of the large AC component of the OHC receptor potential caused by low-frequency sound, which is less attenuated by OHC membrane filter properties. Ca 2+ controls the slow motility of OHCs (Dulon and Schacht 1992;Dulon et al 1990) and, as a consequence, cochlear amplifier activity. According to Patuzzi (2011), very LF sound should be the most effective in eliciting the Bounce as the AC component of OHC receptor potential is large, due to the low-pass filter properties of the OHC membrane.…”

Section: Introductionmentioning

confidence: 99%

Aftereffects of Intense Low-Frequency Sound on Spontaneous Otoacoustic Emissions: Effect of Frequency and Level

Jeanson

Wiegrebe

Gürkov³

et al. 2016

JARO

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The presentation of intense, low-frequency (LF) sound to the human ear can cause very slow, sinusoidal oscillations of cochlear sensitivity after LF sound offset, coined the BBounce^phenomenon. Changes in level and frequency of spontaneous otoacoustic emissions (SOAEs) are a sensitive measure of the Bounce. Here, we investigated the effect of LF sound level and frequency on the Bounce. Specifically, the level of SOAEs was tracked for minutes before and after a 90-s LF sound exposure. Trials were carried out with several LF sound levels (93 to 108 dB SPL corresponding to 47 to 75 phons at a fixed frequency of 30 Hz) and different LF sound frequencies (30, 60, 120, 240 and 480 Hz at a fixed loudness level of 80 phons). At an LF sound frequency of 30 Hz, a minimal sound level of 102 dB SPL (64 phons) was sufficient to elicit a significant Bounce. In some subjects, however, 93 dB SPL (47 phons), the lowest level used, was sufficient to elicit the Bounce phenomenon and actual thresholds could have been even lower. Measurements with different LF sound frequencies showed a mild reduction of the Bounce phenomenon with increasing LF sound frequency. This indicates that the strength of the Bounce not only is a simple function of the spectral separation between SOAE and LF sound frequency but also depends on absolute LF sound frequency, possibly related to the magnitude of the AC component of the outer hair cell receptor potential.

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Increasing intracellular free calcium induces circumferential contractions in isolated cochlear outer hair cells

Cited by 156 publications

References 34 publications

Regeneration of broken tip links and restoration of mechanical transduction in hair cells

Regeneration of broken tip links and restoration of mechanical transduction in hair cells

The Concentrations of Calcium Buffering Proteins in Mammalian Cochlear Hair Cells

Aftereffects of Intense Low-Frequency Sound on Spontaneous Otoacoustic Emissions: Effect of Frequency and Level

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