| ARTICLES |
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| Year : 2003 | Volume
: 5
| Issue : 20 | Page : 19--28 |
Genetic influences in individual susceptibility to noise : A review
RR Davis1, P Kozel2, LC Erway3
1 Hearing Loss Prevention Section, National Institute for Occupational Safety and Health, Cincinnati; Department of Biological Sciences, University of Cincinnati, Cincinnati, OH, USA
2 National Institute of Deafness and Other Communication Disorders, Rockville, MD, USA
3 Department of Biological Sciences, University of Cincinnati, Cincinnati, OH, USA
Correspondence Address:
R R Davis
Hearing Loss Prevention Section, Engineering and Physical Hazards Branch, Division of Applied Research and Technology, National Institute for Occupational Safety and Health. 4676 Columbia Parkway, Cincinnati, OH 45226
USA
 Source of Support: None, Conflict of Interest: None  | Check |
PMID: 14558889 
Individual animals and humans show differing susceptibility to noise damage even under very carefully controlled exposure conditions. This difference in susceptibility may be related to unknown genetic components. Common experimental animals (rats, guinea pigs, chinchillas, cats) are outbred-their genomes contain an admixture of many genes. Many mouse strains have been inbred over many generations raeducing individual variability, making them ideal candidates for studying the genetic modulation of individual susceptibility. Erway et al. (1993) demonstrated a recessive gene associated with early presbycusis in the C57BL/6J inbred mouse. A series of studies have shown that mice homozygous for Ahlallele are more sensitive to the damaging effects of noise.
Recent work has shown that mice homozygous for Ahl are not only more sensitive to noise, but also are probably damaged in a different manner by noise than mice containing the wild-type gene (Davis et al., 2001).
Recent work in Noben-Trauth's lab (Di Palma et al., 2001) has shown that the wild-type Ahl gene codes for a hair cell specific cadherin. Cadherins are calcium dependent proteins that hold cells together at adherins junctions to form tissues and organs. The cadherin of interest named otocadherin or CDH23, is localized to the stereocillia of the outer hair cells. Our working hypothesis, suggests that otocadherin may form the lateral links between stereocilia described by Pickles et al (1989). Reduction of, or missing otocadherin weakens the cell and may allow stereocilia to be more easily physically damaged by loud sounds and by aging.
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