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Outer hair cells extend the hearing range to about 200 kHz in some marine mammals. [16] They have also improved frequency selectivity (frequency discrimination), which is of particular benefit for humans, because it enabled sophisticated speech and music. Outer hair cells are functional even after cellular stores of ATP are depleted. [13]
Hair cells die of old age, acoustic overstimulation and other traumas. [2] Oxotoxin exposure, such as aminoglycoside antibiotics and cisplatin, is also a major contributor to hair cell death. [7] Because mammals have very limited hair cell regeneration, hearing loss is essentially irreversible and therefore a therapeutic target for regeneration.
In hearing, stereocilia transform the mechanical energy of sound waves into electrical signals for the hair cells, which ultimately leads to an excitation of the auditory nerve. Stereocilia are composed of cytoplasm with embedded bundles of cross-linked actin filaments.
Once outer hair cells are damaged, they do not regenerate, and the result is a loss of sensitivity and an abnormally large growth of loudness (known as recruitment) in the part of the spectrum that the damaged cells serve. [13] While hearing loss has always been considered irreversible in mammals, fish and birds routinely repair such damage.
Sensory hearing loss is caused by abnormal structure or function of the hair cells of the organ of Corti in the cochlea. [ disputed – discuss ] Neural hearing impairments are consequent upon damage to the eighth cranial nerve (the vestibulocochlear nerve ) or the auditory tracts of the brainstem .
There are very rare types of hearing loss that affect speech discrimination alone. One example is auditory neuropathy, a variety of hearing loss in which the outer hair cells of the cochlea are intact and functioning, but sound information is not faithfully transmitted by the auditory nerve to the brain. [22]