Low-frequency sound modulates cochlear sensitivity through OHC calcium oscillations

Evidence

The observed effects support the hypothesis that OHC Ca2+ homeostasis is the source of the Bounce: Patuzzi ( 2011 ) suggested that the Bounce is a direct result of OHC activation by LF sound, rather than a secondary effect caused by modulation of stria vascularis activity, as the LF sound-induced endocochlear potential modulation during the Bounce (Kirk and Patuzzi 1997 ) could suggest. Patuzzi ( 2011 ) hypothesized that large, LF-induced receptor potentials in OHCs are the underlying cause of cochlear sensitivity oscillations associated with the Bounce phenomenon. These LF OHC receptor potentials are not attenuated by the low-pass characteristic of the OHC membrane. Patuzzi ( 2011 ) postulated that large, LF receptor potentials activate voltage-sensitive, L-type Ca2+ channels in the OHC membrane. This results in an increase of intracellular Ca2+ in OHCs. Ca2+ -induced Ca2+ release and -uptake mechanisms, with different time courses, can then cause slow, underdamped oscillations of OHC cytosolic Ca2+ concentrations, modulating the gain of the cochlear amplifier (Patuzzi 2011 ). — Dijk, Pim van, Physiology, Psychoacoustics and…, 3747

Categorization

• XREF: Connects to the cochlear amplifier and OHC electromotility literature from inner-ear physiology generally.
• DEEPTHINKING: A specific, falsifiable multi-step mechanism chain — LF receptor potentials driving voltage-gated Ca2+ entry, then underdamped Ca2+ oscillation modulating cochlear gain — is a dense mechanistic model of a normal physiological phenomenon.