Calcium oscillations in outer hair cells drive the hearing Bounce

Evidence

Here, we show that the mechanical amplification of hair cells (OHCs) is significantly affected after the presentation of LF sound. First, we show the Bounce phenomenon in slow level changes of quadratic, but not cubic, distortion product otoacoustic emissions (DPOAEs). Second, Bouncing in response to LF sound is seen in slow, oscillating frequency and correlated level changes of spontaneous otoacoustic emissions (SOAEs). Surprisingly, LF sound can induce new SOAEs which can persist for tens of seconds. Further, we show that the Bounce persists under free-field conditions, i.e. without an in-ear probe occluding the auditory meatus. Finally, we show that the Bounce is affected by contralateral acoustic stimulation synchronised to the ipsilateral LF sound. These findings clearly demonstrate that the origin of the Bounce lies in the modulation of cochlear amplifier gain. We conclude that activity changes of OHCs are the source of the Bounce, most likely caused by a temporary disturbance of OHC calcium homeostasis. In the light of these findings, the effects of long-duration, anthropogenic LF sound on the human inner ear require further research. — Dijk, Pim van, Physiology, Psychoacoustics and…, 3701 (#corroborates, via linked claim)

Patuzzi ( 2011 ) suggested that large receptor-potentials elicited by low-frequency stimulation produce a net Ca2+ influx. The Bounce presumably reflects an underdamped, homeostatic readjustment of increased Ca2+ concentrations and related gain changes after low-frequency sound offset. — Dijk, Pim van, Physiology, Psychoacoustics and…, 3703 (#corroborates, via linked claim)

Patuzzi ( 2011 ) postulated that large, LF receptor potentials activate voltage-sensitive, L-type Ca2+ channels in the OHC membrane. This results in an increase of intracellular Ca2+ in OHCs. Ca2+ -induced Ca2+ release and -uptake mechanisms, with different time courses, can then cause slow, underdamped oscillations of OHC cytosolic Ca2+ concentrations, modulating the gain of the cochlear amplifier (Patuzzi 2011 ). — Dijk, Pim van, Physiology, Psychoacoustics and…, 3703 (#expands, via linked claim)

Categorization

• corroborated: 2 independent passages support this claim
• XREF: connects to: Noise-induced hearing loss begins with impairment of outer hair cells; Low-frequency sound’s after-effects arise from calcium homeostasis in outer hair cells — Dijk, Pim van, Physiology, Psychoacoustics and…, 3701; The SOAE Bounce reflects a calcium-driven homeostatic readjustment in outer hair cells. — Dijk, Pim van, Physiology, Psychoacoustics and…, 3703 (+6 more)

Related

• Low-frequency sound’s after-effects arise from calcium homeostasis in outer hair cells (similarity 0.94)
• The Bounce is a metabolic calcium effect, not mechanical damage to hair cells (similarity 0.93)
• The SOAE Bounce reflects a calcium-driven homeostatic readjustment in outer hair cells. (similarity 0.93)
• Low-frequency exposure measurably alters cochlear amplifier gain via outer hair cell activity (similarity 0.90)
• The olivo-cochlear efferent system accelerates recovery from calcium-induced sensitivity changes. (similarity 0.90)
• Low-frequency receptor potentials drive oscillating calcium levels that modulate cochlear-amplifier gain (similarity 0.90)
• Low-frequency sound modulates cochlear sensitivity through OHC calcium oscillations (similarity 0.88)
• Brainstem efferent signals shorten the hearing Bounce (similarity 0.87)
• The Bounce is caused by OHC calcium homeostasis disruption, not stria damage (similarity 0.87)
• Outer hair cells respond better than inner hair cells to low-frequency sound (similarity 0.87)
• Low-frequency after-effects on inner-ear gain are calcium-mediated and olivocochlear-modulable (similarity 0.85)
• Efferent stimulation maximally suppresses basilar membrane vibration near the characteristic frequency (similarity 0.85)
• The oscillating Bounce cannot be explained by ordinary acoustic overexposure damage (similarity 0.85)
• The oscillating Bounce is metabolic, not damage-linked, unlike ordinary acoustic overexposure (similarity 0.84)
• Low-frequency sound exposure triggers long-lasting damped oscillations in spontaneous otoacoustic emissions. (similarity 0.84)

Broader Connections

• Low-frequency sound’s after-effects arise from calcium homeostasis in outer hair cells #corroborates (0.95) — Dijk, Pim van, Physiology, Psychoacoustics and…, 3701
• The SOAE Bounce reflects a calcium-driven homeostatic readjustment in outer hair cells. #corroborates (0.90) — Dijk, Pim van, Physiology, Psychoacoustics and…, 3703
• Low-frequency receptor potentials drive oscillating calcium levels that modulate cochlear-amplifier gain #expands (0.85) — Dijk, Pim van, Physiology, Psychoacoustics and…, 3703
• Low-frequency sound exposure triggers long-lasting damped oscillations in spontaneous otoacoustic emissions. #expands (0.80) — Dijk, Pim van, Physiology, Psychoacoustics and…, 3703
• Brainstem efferent signals shorten the hearing Bounce #complicates (0.75)
• The olivo-cochlear efferent system accelerates recovery from calcium-induced sensitivity changes. #complicates (0.75) — Dijk, Pim van, Physiology, Psychoacoustics and…, 3744