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
