Low-frequency after-effects on inner-ear gain are calcium-mediated and olivocochlear-modulable

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. … Overall, temporary level reductions of preexisting SOAEs were less pronounced with CAS than without (Wilcoxon signed rank test, p = 0.085 and 0.007 for CAS levels of 65 and 70 dB, respectively), while the SOAE level increases remained fairly unchanged. This resulted in a less symmetrical shape of the SOAE Bounce compared to the reference recording. Consequently, the time constants of the fitted function with CAS shortened significantly. — Dijk, Pim van, Physiology, Psychoacoustics and…, 3736

Categorization

• XREF: Connects to the earlier concept of the Bounce following low-frequency sound (chapter on post-stimulatory effects) and to theories that OHC electromotility set-point homeostatically re-regulates after overstimulation.
• QUESTION: Why did CAS suppress the level-reduction (unadapted) phase but leave the level-increase phase unchanged, and can this asymmetry identify two distinct underlying mechanisms rather than one homeostatic loop?