The Bounce is caused by OHC calcium homeostasis disruption, not stria damage

Evidence

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. 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. — Dijk, Pim van, Physiology, Psychoacoustics and…, 3744

Categorization

• DEFINE: Clarifies what the Bounce phenomenon is and its hypothesized cellular mechanism.
• QUESTION: Worth verifying whether the Bounce phenomenon’s Ca2+ hypothesis is settled or still debated in later literature.