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Inner ear regeneration is the biological process by which the hair cells and supporting cells (i.e. Hensen's cells and Deiters cells) of the ear proliferate (cell proliferation) and regrow after hair cell injury. This process depends on communication between supporting cells and the brain.
[5] [6] Furthermore, Hensen's cells are also able to regenerate the damaged hair cells in some vertebrates; they undergo phagocytosis to eject the dead or injured hair cells, and reproduce both new hair cells and supporting cells into the cell cycle. One of the reasons is that the supporting cells are differentiated by the embryonic hair cells ...
While hair cells are generally not replaced through cell regeneration, [131] mechanisms are being studied to induce replacement of these important cells. [132] One study involves the replacement of damaged hair cells with regenerated cells, via the mechanism of gene transfer of atonal gene Math1 to pluripotent stem cells within the inner ear ...
The cell cycle inhibitor p27kip1 has also been found to encourage regrowth of cochlear hair cells in mice following genetic deletion or knock down with siRNA targeting p27. [36] [37] Research on hair cell regeneration may bring us closer to clinical treatment for human hearing loss caused by hair cell damage or death.
The outer hair cells, instead, mainly 'receive' neural input from the brain, which influences their motility as part of the cochlea's mechanical "pre-amplifier". The input to the OHC is from the olivary body via the medial olivocochlear bundle. The cochlear duct is almost as complex on its own as the ear itself.
In the semicircular canals, the hair cells are found in the crista ampullaris, and the stereocilia protrude into the ampullary cupula. Here, the stereocilia are all oriented in the same direction. In the otoliths, the hair cells are topped by small, calcium carbonate crystals called otoconia. Unlike the semicircular ducts, the kinocilia of hair ...
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Age-related hair cell degeneration is characterized by loss of stereocilia, shrinkage of hair cell soma, and reduction in outer hair cell mechanical properties, suggesting that functional decline in mechanotransduction and cochlear amplification precedes hair cell loss and contributes to age-related hearing loss.