Mechanism of cochlear lateral wall fibrocytes regeneration

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Our research aimed to reveal the mechanism of cochlear lateral wall regeneration after severe damage caused by acute mitochondrial dysfunction. First, we successfully made a mouse model of acute mitochondrial dysfunction used by 3-nitropropionic acid (3-NP). This mouse model had severe hearing loss measured by auditory brainstem response (ABR), which was caused by apotosis on the cochlear lateral wall fibrocytes. Two months after 3-NP administration, spontaneous ABR threshold recovery was observed. Moreover, endocochlear potential was also recovered at the same timing. Therefore, regeneration of cochlear lateral wall fibrocytes leads to recovery of endocochlear potential, following recovery of hearing.