The SOAE Bounce reflects a calcium-driven homeostatic readjustment in outer hair cells.

Evidence

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

Categorization

• DEFINE: Defines the mechanism behind the Bounce phenomenon in terms of OHC calcium homeostasis.
• corroborated: 3 independent passages support this claim — Dijk, Pim van, Physiology, Psychoacoustics and…, 3703
• XREF: connects to: Calcium oscillations in outer hair cells drive the hearing Bounce; The Bounce is a metabolic calcium effect, not mechanical damage to hair cells; Low-frequency sound’s after-effects arise from calcium homeostasis in outer hair cells — Dijk, Pim van, Physiology, Psychoacoustics and…, 3701 (+2 more)

Broader Connections

• The Bounce is a metabolic calcium effect, not mechanical damage to hair cells #expands (0.95)
• Low-frequency sound’s after-effects arise from calcium homeostasis in outer hair cells #exemplifies (0.90) — Dijk, Pim van, Physiology, Psychoacoustics and…, 3701
• SOAE bouncing is not caused by middle-ear impedance changes #corroborates (0.85)
• The olivo-cochlear efferent system accelerates recovery from calcium-induced sensitivity changes. #responds-to (0.80) — Dijk, Pim van, Physiology, Psychoacoustics and…, 3744