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Abstract Many people have suprathreshold auditory processing difficulties despite normal audiometric thresholds, referred to as “hidden hearing loss.” Such difficulties are widely thought to originate from pathology of the inner hair cell ribbon synapse (cochlear synaptopathy) following noise-exposure-induced temporary threshold shifts. This pathology impairs the temporally-precise sound encoding necessary for spatial hearing, but direct evidence in primates, human or nonhuman, is lacking.
Abstract Medial olivocochlear (MOC) efferents modulate outer hair cell motility through specialized nicotinic acetylcholine receptors to support encoding of signals in noise. Transgenic mice lacking the alpha9 subunits of these receptors (a9KOs) have normal hearing in quiet and noise, but lack classic cochlear suppression effects and show abnormal temporal, spectral, and spatial processing.
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