Involvement of apoptosis in progression of cochlear lesion following exposure to intense noise.
It has been known for some time that noise-induced outer hair cell (OHC) death in the cochlea continues well after the termination of a noise exposure. However, the underlying mechanisms leading to the expansion of a cochlear lesion are not fully understood. Here we report involvement of the apoptotic pathway in the progression of OHC death in the chinchilla cochlea following exposure to a 4 kHz narrow band noise at 110 dB SPL for 1 h. Morphological examination of OHC nuclei revealed nuclear condensation and fragmentation, typical morphological features of apoptosis. OHC apoptosis developed asymmetrically toward the apical and basal parts of the cochleas following the noise exposure. Two days after the noise exposure, there was still active OHC pathology with condensed and fragmented nuclei in the basal part of the cochleas. Detection of caspase-3 activation, an intracellular marker for apoptosis, showed a spatial agreement between the apoptotic nuclei and activated caspase-3. These results clearly implicate the apoptotic pathway in the post-exposure progression of OHC demise.
Hu
Bo Hua
BH
Center for Hearing and Deafness, Department of Communicative Disorders and Sciences, State University of New York at Buffalo, 215 Parker Hall, 3435 Main Street, Buffalo, NY 14214, USA.
Henderson
Donald
D
Nicotera
Thomas M
TM
D000818:Animals; D017209:Apoptosis; D053148:Caspase 3; D020169:Caspases / Q000378:metabolism; D002467:Cell Nucleus / Q000473:pathology; D002682:Chinchilla; D003051:Cochlea / Q000201:enzymology / Q000293:injuries* / Q000473:pathology*; D004789:Enzyme Activation; D005456:Fluorescent Dyes; D018072:Hair Cells, Auditory, Outer / Q000201:enzymology / Q000473:pathology; D006317:Hearing Loss, Noise-Induced / Q000201:enzymology / Q000473:pathology*; D018613:Microscopy, Confocal; D008856:Microscopy, Fluorescence; D011419:Propidium
D005456:Fluorescent Dyes; D011419:Propidium; D053148:Caspase 3; D020169:Caspases