GENETICS OF AGE-RELATED HEARING-LOSS IN MICE .3. SUSCEPTIBILITY OF INBRED AND F1-HYBRID STRAINS TO NOISE-INDUCED HEARING-LOSS

Citation
Lc. Erway et al., GENETICS OF AGE-RELATED HEARING-LOSS IN MICE .3. SUSCEPTIBILITY OF INBRED AND F1-HYBRID STRAINS TO NOISE-INDUCED HEARING-LOSS, Hearing research, 93(1-2), 1996, pp. 181-187
Citations number
21
Categorie Soggetti
Neurosciences,Acoustics
Journal title
ISSN journal
03785955
Volume
93
Issue
1-2
Year of publication
1996
Pages
181 - 187
Database
ISI
SICI code
0378-5955(1996)93:1-2<181:GOAHIM>2.0.ZU;2-7
Abstract
Some humans and mice are genetically predisposed to age-related hearin g loss (AHL), and others are variously susceptible to noise-induced he aring loss (NIHL). The inbred C57BL/6J (B6) mice exhibit AHL at an ear ly age, whereas the inbred CBA/CaJ (CB) mice do not. The B6 mice are m uch more susceptible to NIHL than are the CB mice (Shone et al., 1991; Li, 1992a). The B6 mice possess an Ahl gene which maps to chromosome 10 (Erway et al., 1995). This study was designed, using these two inbr ed strains plus two F1 hybrid strains of mice, to begin to test the hy pothesis that the Ahl genotypes may influence the susceptibility to NI HL. These strains of mice (with putative genotypes) are: inbred CB (+/ +) and B6 (Ahl/Ahl); hybrid CBBBF1 (+/Ahl) and B6D2F1 (Ahl/Ahl; D2 rep resents inbred DBA/2J). Twenty-four mice of each of these four strains were exposed to noise (110 dB for 0, 1 or 2 h) and tested for auditor y-evoked brainstem response (ABR) thresholds. The CB and CBB6F1 strain s of mice did not differ significantly from each other, exhibiting mos tly temporary threshold shifts. The B6 and B6D2F1 strains of mice did not differ significantly from each other, but did exhibit permanent th reshold shifts. These results support the hypothesis that genetic pred isposition to AHL may be revealed at a younger age by NIHL. This sugge sts that it may be possible to use the NIHL to distinguish segregating genotypes (+/Ahl vs. Ahl/Ahl) among backcross progeny and thereby to identify and map single genes for AHL.