Aging outer hair cells (OHCs) in the Fischer 344 rat cochlea: function and morphology.
As previously reported [Popelar, J., Groh, D., Pelanova, J., Canlon, B., Syka, J., 2006. Age-related changes in cochlear and brainstem auditory functions in Fischer 344 rats. Neurobiol. Aging 27, 490-500; Buckiova, D., Popelar, J., Syka, J., 2007. Aging cochleas in the F344 rat: morphological and functional changes. Exp. Gerontol. 42, 629-638; Bielefeld, E.C., Coling, D., Chen, G.D., Li, M.N., Tanaka, C., Hu, B.H., Henderson, D., 2008. Age-related hearing loss in the Fischer 344/NHsd rat substrain. Hear. Res. 241, 26-33], aged Fischer 344 (F344) rats with severe hearing loss retain many outer hair cells (OHCs) especially in the middle turn of the cochlea. The current study confirmed the previous findings showing that aged OHCs were present, but dysfunctional. Distortion product otoacoustic emissions (DPOAE), which are believed to reflect in vivo OHC motility, were absent in the aged rats while the majority of OHCs (>80%) were present and morphologically intact. There was no detectable injury of OHC stereocilia as assessed by actin-staining and examination under the light microscope. Cochlear microphonics (CM) at 12kHz, recorded from the middle turn, only showed a slight age-related reduction, indicating a normal mechanoelectrical transduction apparatus in the remaining OHCs in the cochlear regions with 10-20% OHC loss. Activities of succinate dehydrogenase (SDH), an enzyme shared by the citric acid cycle and the mitochondrial electron transport chain (METC), were also at normal levels in aged OHCs. Importantly, aged OHCs showed reduced levels of prestin immunolabeling compared to young controls. Together with our previous finding showing that the stria vascularis and endocochlear potential were essentially normal in aged F344 rats [Bielefeld, E.C., Coling, D., Chen, G.D., Li, M.N., Tanaka, C., Hu, B.H., Henderson, D., 2008. Age-related hearing loss in the Fischer 344/NHsd rat substrain. Hear. Res. 241, 26-33], the results suggest that disruption of prestin is the major cause of DPOAE loss and loss of cochlear sensitivity.
Chen
Guang-Di
GD
Center for Hearing and Deafness, SUNY at Buffalo, NY 14214, USA. gchen7@buffalo.edu
Li
Manna
M
Tanaka
Chiemi
C
Bielefeld
Eric C
EC
Hu
Bo-Hua
BH
Kermany
Mohammad Habiby
MH
Salvi
Richard
R
Henderson
Donald
D
D000200:Action Potentials; D000375:Aging / Q000502:physiology*; D000818:Animals; D027321:Anion Transport Proteins / Q000378:metabolism; D002452:Cell Count; D002923:Cilia / Q000648:ultrastructure; D003051:Cochlea / Q000166:cytology* / Q000502:physiology; D003055:Cochlear Microphonic Potentials; D004594:Electrophysiology; D006198:Hair Cells, Auditory / Q000166:cytology; D018072:Hair Cells, Auditory, Outer / Q000166:cytology* / Q000502:physiology*; D007150:Immunohistochemistry / Q000379:methods; D017084:Otoacoustic Emissions, Spontaneous; D010469:Perceptual Distortion; D051381:Rats; D011916:Rats, Inbred F344 / Q000502:physiology*; D020318:Rats, Long-Evans; D011984:Sensory Receptor Cells / Q000502:physiology; D013194:Staining and Labeling; D013316:Stria Vascularis / Q000502:physiology; D013385:Succinate Dehydrogenase / Q000378:metabolism; D000076988:Sulfate Transporters
D027321:Anion Transport Proteins; C409207:Slc26a5 protein, rat; D000076988:Sulfate Transporters; D013385:Succinate Dehydrogenase