The Bounce is not acoustic damage because overexposure recovery is monotonic, not oscillatory

Evidence

As the low-frequency stimuli used in this study are intense, mechanisms associated with acoustic overexposure and recovery thereof could in principle be responsible for the Bounce phenomenon. Temporary or permanent damage to OHCs represent an unlikely cause, as recovery from acoustic overexposure with sounds in the sensitive range of hearing is typically monotonic, does not oscillate and no hypersensitivity can be seen. It has been shown, however, that intense sound stimulation of the cochlea in the isolated temporal bone preparation increases intracellular Ca2+ level of hair cells and supporting cells (Fridberger et al. 1998 ; Jacob et al. 2013 ). Acoustic injury consists of a plethora of structural and metabolic changes to the cochlea, with structural damage possibly masking more subtle (and possibly oscillating) metabolic changes of cochlear sensitivity caused by the rise of intracellular Ca2+ levels. — Dijk, Pim van, Physiology, Psychoacoustics and…, 3746

Categorization

Category: Causal Relationships

• QUESTION: Structural damage could be masking oscillating metabolic calcium-driven sensitivity shifts — what would a non-masking experiment look like?

Related

• The oscillating Bounce cannot be explained by ordinary acoustic overexposure damage (similarity 0.96)
• Recovery from acoustic overexposure is monotonic and shows no hypersensitivity (similarity 0.95)
• The oscillating Bounce is metabolic, not damage-linked, unlike ordinary acoustic overexposure (similarity 0.95)
• The Bounce is caused by OHC calcium homeostasis disruption, not stria damage (similarity 0.91)
• Intense cochlear sound stimulation raises intracellular calcium in hair cells (similarity 0.84)
• Calcium oscillations in outer hair cells drive the hearing Bounce (similarity 0.83)
• The Bounce is a metabolic calcium effect, not mechanical damage to hair cells (similarity 0.83)
• Low-frequency sound’s after-effects arise from calcium homeostasis in outer hair cells (similarity 0.83)
• Low-frequency sound modulates cochlear sensitivity through OHC calcium oscillations (similarity 0.82)
• The SOAE Bounce reflects a calcium-driven homeostatic readjustment in outer hair cells. (similarity 0.82)
• Low-frequency exposure measurably alters cochlear amplifier gain via outer hair cell activity (similarity 0.81)
• The SOAE Bounce arises from homeostatic correction of low-frequency-induced calcium influx (similarity 0.80)
• Repeated noise overexposure converts temporary threshold shifts into permanent hearing loss (similarity 0.79)
• Low-frequency after-effects on inner-ear gain are calcium-mediated and olivocochlear-modulable (similarity 0.78)
• The olivo-cochlear efferent system accelerates recovery from calcium-induced sensitivity changes. (similarity 0.78)