Brainstem efferent signals shorten the hearing Bounce

Evidence

In contrast, the slow efferent effect (Sridhar et al. 1997 ) can cause a constant Ca2+ release from OHC internal stores, the lateral cisternae, while CAS is on. We hypothesize that this constant influx of Ca2+ may help to accelerate Ca2+ -dependent Ca2+ -uptake and thus, a quicker recovery of the system. In summary, the current experiments reveal a pronounced effect of LF exposure on the active mechanisms in the inner ear, as they are mediated by OHCs. — Dijk, Pim van, Physiology, Psychoacoustics and…, 3744 (#expands, via linked claim)

Categorization

• XREF: connects to: Brain efferents can dynamically adjust cochlear gain during listening; Calcium oscillations in outer hair cells drive the hearing Bounce; The Bounce is not ordinary acoustic-overexposure recovery (+2 more)

Related

• The olivo-cochlear efferent system accelerates recovery from calcium-induced sensitivity changes. (similarity 0.93)
• Calcium oscillations in outer hair cells drive the hearing Bounce (similarity 0.87)
• Efferent stimulation maximally suppresses basilar membrane vibration near the characteristic frequency (similarity 0.86)
• Low-frequency after-effects on inner-ear gain are calcium-mediated and olivocochlear-modulable (similarity 0.85)
• Low-frequency receptor potentials drive oscillating calcium levels that modulate cochlear-amplifier gain (similarity 0.84)
• Brain efferents can dynamically adjust cochlear gain during listening (similarity 0.84)
• Low-frequency sound modulates cochlear sensitivity through OHC calcium oscillations (similarity 0.84)
• The SOAE Bounce reflects a calcium-driven homeostatic readjustment in outer hair cells. (similarity 0.83)
• The SOAE Bounce arises from homeostatic correction of low-frequency-induced calcium influx (similarity 0.82)
• Medial olivocochlear efferents actively modulate cochlear gain during binaural listening (similarity 0.81)
• Low-frequency sound’s after-effects arise from calcium homeostasis in outer hair cells (similarity 0.80)
• Cochlear amplifier gain oscillates via underdamped OHC calcium cycling (similarity 0.80)
• The Bounce is caused by OHC calcium homeostasis disruption, not stria damage (similarity 0.80)
• Low-frequency exposure measurably alters cochlear amplifier gain via outer hair cell activity (similarity 0.79)
• The oscillating Bounce cannot be explained by ordinary acoustic overexposure damage (similarity 0.79)

Broader Connections

• The olivo-cochlear efferent system accelerates recovery from calcium-induced sensitivity changes. #expands (0.82) — Dijk, Pim van, Physiology, Psychoacoustics and…, 3744
• Signal durations under the efferent onset delay isolate the efferent effect on cochlear gain #qualifies (0.75)