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This transient, noise-induced paradoxical phenomenon, which precedes the eventual silencing of auditory nerve fibers and synapses, may be characterized by (1) excessive glutamate release from IHCs, resulting in overactivation of receptors on auditory nerve fibers 66 , and (2) functional compensation by LOC efferent neurons, ensuring that auditory nerve activity is enhanced during periods of increased demand 67 , consistent with evidence suggesting that a primary function of LOC efferents is to reduce auditory neuropathy 68
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