作者: Qunfeng Cai , Bo Wang , Donald Coling , Jian Zuo , Jie Fang
DOI: 10.1371/JOURNAL.PONE.0113990
关键词:
摘要: Various cochlear pathologies, such as acoustic trauma, ototoxicity and age-related degeneration, cause hearing loss. These pre-existing losses can alter responses to subsequent overstimulation. So far, the knowledge on impacts of loss caused by genetic alteration genes is limited. Prestin motor protein expressed exclusively in outer hair cells mammalian cochlea. This contributes cell motility. At present, it not clear how interference prestin function affects To address this question, a model dysfunction mice was created inserting an internal ribosome entry site (IRES)-CreERT2-FRT-Neo-FRT cassette into locus after stop codon. Homozygous exhibit threshold elevation auditory brainstem with large individual variation. also display shift input/output distortion product otoacoustic emission, suggesting reduction function. The disruption reduces shifts exposure loud noise at 120 dB (sound pressure level) for 1 h. positively correlated level pre-noise accompanied reduced change Cdh1 expression, molecular Together, these results suggest that stress