Protection By Sound Conditioning From Acoustic Trauma And Its Mechanism

AIM: The changes in cochlear hair cells following sound conditioning were observed, and effects of changes in morphology, cytoskeleton and intracellular calcium homeostasis on audition and its mechanism were investigated in order to provide the experimental data for elucidating the mechanism of sound conditioning and preventing noise-induced hearing loss. METHODS: Forty healthy guinea pigs with normal Preyer's reflex were used in the study. The animals were randomly divided into four groups: normal group(NG), conditioning noise group(CG), high-level noise group(HG) and conditioning noise followed by high-level noise group(CHG). Sound conditioning experimental model of animals was established. ABR threshold was tested with auditory electrical physiology method. Hair cell loss was measured using surface preparation technique in morphological aspect, and the immunoreactivities of CaM. HSP70 and F-actin in hair cells were examined with the method of immunohistochemistry. At the same time, free calcium concentration was observed in hair cells using LSCM. Microphotographics and image analysis were also used for quantitative investigation. RESULTS: 1. In the present study, Sound conditioning experimental model of animals was established successfully. Conditioning noise exposure protected hearing loss by 13dB from an acoustic trauma that resulted in the following high-level noise exposure. 2. Cochlear surface preparations indicated that the loss of hair cells induced by noise exposure was obvious. A significant difference was observed between group HG and group CHG at the first and the second turn of the basilar membrane. 3. The expression of CaMK HSP70 and F-actin all showed anABSTRACTincreased trend after noise exposure, and changed similarly in all the groups. HSP70 and F-actin expressed significantly more in group CHG than that expressed in group HG. Compaired with group HG, the expression of CaM showed an increased trend in group CHG. 4. Intracellular calcium concentration could be elevated resulted from noise exposure. In group HG, the calcium concentration was significantly higher than that in group CG and group CHG. CONCLUSION: 1. Sound conditioning experimental model of animals was established successfully with appropriate noise conditions. 2. Morphological changes in hair cell stem from noise exposure includes hair cell loss and other impairments instead of hair cell death. Sound conditioning can decrease hair cell loss induced by the following high-level noise exposure. 3. A suitable sound conditioning can make the auditory system of guinea pig more resistant to noise trauma. For example, the expression of Ca/U HSP70 and F-actin increase in hair cell. 4. Intracellular calcium overloading is one of the most important mechanisms of noise-induced hearing loss. The strengthened cytoskeleton system and the intracellular calcium homeostasis play a critical role in the protective mechanism of sound conditioning.