ABSTRACT
Permanent hearing loss by noise exposure is the functional consequence of a complex set of pathological changes in the cochlea. Among these changes, hair cell (HC) death may contribute most to the loss of auditory function. It has been known that noise-induced HC death starts during a noise exposure and continues even after the termination of the noise exposure. Biological mechanisms underlying the progression of HC death are not fully understood. Here we describe progression of HC death in the chinchilla cochlea after exposure to a 4-kHz narrow band noise at 110 dB sound pressure level (SPL) for 1 hour. Morphological examination of HC nuclei revealed typical nuclear changes for both apoptosis and necrosis. Apoptosis appeared to be a major death pathway leading to progression of the cochlear lesion in noise-damaged cochleas. The study also showed that expansion of HC death developed asymmetrically toward the apical and basal parts of the cochleas. Detection of caspase-3 activation showed a spatial agreement between the apoptotic nuclear changes and caspase-3 activation. These results clearly implicate the apoptotic pathway in the postexposure progression of HC demise.
KEYWORDS
Noise - hair cell - apoptosis - cochlea
