The Bounce is a metabolic calcium effect, not mechanical damage to hair cells

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)

Loss of outer hair cells impacts the shape and slope of the basilar membrane I-O function in a way very similar to loudness growth functions measured in listeners with SNHL. This correlation and the presence of loudness recruitment in listeners with mild and moderate hearing losses, who presumably have predominantly outer hair cell loss, suggest that loss of outer hair cells contributes to loudness recruitment. — Jennifer Lentz, Psychoacoustics- Perception of Normal…, 851 (#complicates, via linked claim)

Categorization

• XREF: connects to: The Bounce is not ordinary acoustic-overexposure recovery; The SOAE Bounce reflects a calcium-driven homeostatic readjustment in outer hair cells. — Dijk, Pim van, Physiology, Psychoacoustics and…, 3703; Calcium oscillations in outer hair cells drive the hearing Bounce (+2 more)

Related

• Low-frequency sound’s after-effects arise from calcium homeostasis in outer hair cells (similarity 0.94)
• Calcium oscillations in outer hair cells drive the hearing Bounce (similarity 0.93)
• Low-frequency exposure measurably alters cochlear amplifier gain via outer hair cell activity (similarity 0.91)
• The SOAE Bounce reflects a calcium-driven homeostatic readjustment in outer hair cells. (similarity 0.89)
• Outer hair cells respond better than inner hair cells to low-frequency sound (similarity 0.89)
• Outer hair cell loss is the primary driver of loudness recruitment (similarity 0.88)
• Noise-induced hearing loss begins with impairment of outer hair cells (similarity 0.84)
• The Bounce is caused by OHC calcium homeostasis disruption, not stria damage (similarity 0.84)
• The oscillating Bounce is metabolic, not damage-linked, unlike ordinary acoustic overexposure (similarity 0.84)
• The oscillating Bounce cannot be explained by ordinary acoustic overexposure damage (similarity 0.84)
• Recovery from acoustic overexposure is monotonic and shows no hypersensitivity (similarity 0.83)
• The Bounce is not acoustic damage because overexposure recovery is monotonic, not oscillatory (similarity 0.83)
• The olivo-cochlear efferent system accelerates recovery from calcium-induced sensitivity changes. (similarity 0.82)
• Active outer hair cell processing boosts internal response levels by up to 40 dB (similarity 0.82)
• SOAE bouncing is not caused by middle-ear impedance changes (similarity 0.81)

Broader Connections

• Calcium oscillations in outer hair cells drive the hearing Bounce #corroborates (1.00)
• Low-frequency sound’s after-effects arise from calcium homeostasis in outer hair cells #corroborates (0.95) — Dijk, Pim van, Physiology, Psychoacoustics and…, 3701
• Outer hair cell loss is the primary driver of loudness recruitment #complicates (0.75) — Jennifer Lentz, Psychoacoustics- Perception of Normal…, 851