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Objective To study the general mechanical behavior pattern of sensing angular velocity by 3 pairs of human semicircular canals.Methods Sinusoidal head rotation of a healthy subject was simulated by finite element method to analyze the dynamic responses in the above 3 pairs of canals in the left and right inner ear.Results Compared with the complicated node displacement distribution,the volumetric strain distribution of cupula was regular.Specifically,each pair of cupulae expanded or contracted within the same amplitude with the same response frequency to the angular velocity.The ratio of absolute volumetric strain among the horizontal semicircular canal cupula (HC cupula),the anterior semicircular canal cupula (AC cupula),and the posterior semicircular canal cupula (PC cupula),was approximately 1.00∶0.80 ∶ 1.72,which kept constant.In addition,the volumetric strain of HC cupula was in phase with that of AC cupula,but showing 14.4° out of phase with the angular velocity,and 180° out of phase with that of PC cupula.Conclusions The volumetric strain of cupula can preferably characterize the directional coding function of semicircular canal,and the amplitude,frequency and phase of the cupular volumetric strain can encode those of the stimulated angular velocity,respectively.These results will lay the foundation for establishing quantitative relationship of vestibulo-ocular reflex,and provide theoretical references for quantitative assessment for vestibular function by nystagmus examination.
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Objective In this study ,we investigated the apoptosis of hair cell in the cochlea of age -related hearing loss(AHL) generated by ENU mutagenesis ,and to study a pan caspase inhibitor (z-VAD -FMK) which is to protect the cochlea hair cells from hearing loss induced by age-related hearing loss(AHL) .Methods Through z-VAD-FMK intraperitoneal injection and round window membrane (RWM) drug were delivered into the Cdh23 nmf308 nmf/nmf mice 5(postnatal days 2 -32) inner ear .ResuIts The results showed that the nmf308 mice with progressive hair cell loss along a base to apex gradient with age-related hearing loss .The cochlear OHCs reduced from 5% ~10% at 1 month to 100% at 3 month in the basal region .Substantial amounts of TUNEL -positive OHCs nuclei appeared at 1 month age ,and activated caspase-3 labeling demonstrated that most OHCs appeared at 2 months age .These suggested that DNA single strand break was attributed primarily to apoptosis of cochlear le_sions ,whereas in the later stage of lesion ,the expansion led to activation of caspase-3 activity reduced with further progression of nuclear condensation in age-related hearing loss .ConcIusion The addition of a pan caspase inhibitor (z -VAD -FMK ) significantly protected the cochlea against the hair cell loss induced by apoptosis .Our study showed that aspase inhibitor ,Z-VAD-FMK appeared to play a prominent role in age-related hearing loss media_ted hair cell death loss induced by apoptosis .Our study showed that aspase inhibitor ,Z-VAD -FMK appeared to play a prominent role in age-related hearing loss mediated hair cell death .
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Objective In this study,we investigated the hair cell apoptosis and the molecular mechanisms in age-related hearing IOSS mouse cochlea.Methods All animals were assessed by ABR and DPOAE analysis in both ears.TUNEL(Terminal dexynucleotidyl transferase(TdT)mediated dUTP Nick End Labeling)and PI were used to identify DNA fiagments and caspase-3 activities in hair cells.Results The results showed that the nmf308 mice had progressive hair cell loss along with age.The cochlear OHCs were reduced 5%～10% at 1 month and 100% at 3 month in the basal region.Substantial amounts of TUNEL-postive OHCs nuclei were observed at age of 1 month,and activated caspase-3 labeling OHCs were most obviously observed at age of 2 months.Conclusion These results suggest that DNA single strand break is attributed primarily to apoptosis of cochlear lesion,and activation of caspase-3 at leter stage leads to the hair cell apoptiovs of nuclear condensation in age-related hearing loss mouse cochlea.
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Objective To study the recovery of the outer hair cells in the bat cochlea after gentamicin exposure.Methods Bats were injected with a daily dose of gentamicin for 15 consecutive days and bromodeoxyuridine (BrdU)was given from day 16 to day 40 of this recovery phase. Hearing was assessed by overt acoustic behavior and auditory brainstem responses analysis, which was performed one day prior to the first injection and a day after the last injection (day 16). On day 40 animals were sacrificed for detection of cells that could take up BrdU. Results After 15 days of gentamicin treatment, all of the animals were proved to be deafened with significant increases of ABR thresholds,compared with control group. The findings in immunocytochemical stained samples and scanning electron microscopy revealed that BrdU labeled nuclei were observed in the cochlea in all of the deafened animals most commonly in the regions of the first-row and second-row Deiter's cells (DCs) and occasionally in the regions of the third-ruw DCs.Conclusion We suggest that, under sufficient drug and enough time, the bat cochlear supporting cells can directly transdifferentiate into the outer hair cells after aminoglycoside exposure. This transdifferentation process is essential for repair of outer hair cells and recovery of normal function after gentamicin exposure.