Experimental Observation Of Auditory Physiology And Cochlea Morphology In TGF～β/Smad5 Gene Knockout Mice

Part one: Experimental observation of auditory physiology and cochlea morphology in TGF~/Smad5 gene knockout miceObjective: To observe the changes of auditory physiology and cochlea morphology in TGF~/Smad5 gene knockout mice, and to explore whether Smad5 is a new related gene to hearing function. Methods: Use double blind control methods to conduct auditory physiology method (ABR, DPOAE) and make experimental observation on cochlea morphology (cochlea frozen-cut section and surface preparation) in the mouse of Smad5 (+/+) and Smad5(+/-). The hair cell count was also taken. Results: As shown by ABR , the average hearing of Smad5 (+/-) mouse (aged 12 weeks) was 90.63 17.65 dB (SPL) and that of Smad5(+/+) mouse was 63 19.94 dB(SPL), which were of significant difference (P<0.01). DPOAE was not induced in Smad5 (+/-) mouse (aged 12 weeks) and was normally induced in Smad5 (+/+) mouse. As shown by frozen-cut section and surface preparation, outer hair cells became deficient in Smad5 (+/-) mouse (especially in its basal turn) but became only slightly deficient in Smad5 (+/+) mouse, The comparison of outer hair cell count between Smad5 (+/-) mouse and Smad5 (+/+) mouse indicated a significant difference (P<0.01). However, the comparison of inner hair cell count between Smad5 (+/-) mouse and Smad5 (+/+) mouse indicated no significant difference (P>0.05). Conclusion: TGF~/ Smad5( + /-) gene knockout can cause, to moderate or severe extent, the increase in auditory threshold of mouse. Cochlea morphology indicates that hair cells (mainly outer hair cells) in mouse cochlea basal turn become deficient. Amechanism of TGF~β/Smad5 gene knockout to cause the deafness and thedeficiency of hair cells still requires a further research.