The SOAE Bounce arises from homeostatic correction of low-frequency-induced calcium influx

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. Here, we tested this hypothesis by activating the medial olivocochlear (MOC) efferent system during presentation of the Bounce-evoking LF sound. The MOC system is known to modulate OHC Ca2+ concentrations (Sridhar et al. 1997 ) and receptor potentials (Fex 1967 ) and therefore it should modulate the characteristics of the Bounce. — Dijk, Pim van, Physiology, Psychoacoustics and…, 3736

Categorization

• QUESTION: If Ca2+ flux is the mechanism, what dose-response and temperature-dependence does this predict for the Bounce’s time constants?