摘要
It has been revealed in recent years that contralateral acoustic stimulation can affect cochlear active mechanisms through activating medial olivocochlear system (MOC) of the cochlear efferent nerve fibers. The MOC is therefore postulated to exert protective effects on outer hair cells (OHCs) under intense sound condition. In this study the effects of 4 kHz intense tone exposure on distortion product otoacoustic emissions (DPOAEs) in guinea pigs with and without contralateral white noise stimulation were observed so that to investigate the protective effects of MOC on OHCs. The results showed that DPOAEs obviously deceased after the intense tone exposure in all animals, while both the amplitude reduction and the affected frequency range of DPOAEs were smaller in animals with simultaneously delivered contralateral white noise during the tone exposure than that in animals without colltralateral acoustic stimulation. The above results may suggest some protective nature of the contralateral sound stimulating effects which might be mediated through the activity of MOC. These perhaps can serve as the evidence that the protective mechanism against intense sound operates in the outer hair cells which are strongly innervated by MOC
It has been revealed in recent years that contralateral acoustic stimulation can affect cochlear active mechanisms through activating medial olivocochlear system (MOC) of the cochlear efferent nerve fibers. The MOC is therefore postulated to exert protective effects on outer hair cells (OHCs) under intense sound condition. In this study the effects of 4 kHz intense tone exposure on distortion product otoacoustic emissions (DPOAEs) in guinea pigs with and without contralateral white noise stimulation were observed so that to investigate the protective effects of MOC on OHCs. The results showed that DPOAEs obviously deceased after the intense tone exposure in all animals, while both the amplitude reduction and the affected frequency range of DPOAEs were smaller in animals with simultaneously delivered contralateral white noise during the tone exposure than that in animals without colltralateral acoustic stimulation. The above results may suggest some protective nature of the contralateral sound stimulating effects which might be mediated through the activity of MOC. These perhaps can serve as the evidence that the protective mechanism against intense sound operates in the outer hair cells which are strongly innervated by MOC
