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Noise exposure induced cochlear hair cell death pathways in guinea pig

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Journal of Otology 2010年第1期5卷 51-56页

作者： alfred nuttall Oregon Hearing Research Center KHRI University of Michigan

Objective To understand the mechanism of noise exposure induced outer hair cells(OHCs) death pathways. Methods Thirty two guinea pigs were used in this study. The animals were either exposed for 4 h/day to broadband noise at 122 dB SPL (A-weighted) for 2 consecutive days or perfused with MNNG. After auditory test, the cochleae of animals were dissected. Propidium iodide (PI), a DNA intercalating fluorescent probe, was used to trace morphological changes in OHC nuclei. F-actin staining was used to determine missing OHCs. Caspase-3 was detected in living organ of Corti whole mounts using the fluorescent probe. The single strand DNA (ssDNA) in apoptotic OHCs in guinea pigs and apoptosis inducing factor (AIF) in hair cells in guinea pigs were examined by immunohistology method. Whole mounts of organ of Corti were prepared. Morphological and fluorescent changes were examined under a confocal microscope. Results (1) Both apoptotic and necrotic hair cells appeared following noise exposure. (2) Noise exposure induced single strand DNA in apoptotic OHCs but not in the normal OHCs. (3) Either after noise exposure or after MNNG perfusion, apoptotic OHCs were featured by nuclear condensation or fragmentation with caspase-3 activation, whereas necrotic OHCs were characterized by nuclear swelling without caspase-3 activation. (4) In normal organ of Corti, AIF was located in the mitochondria areas. After noise exposure, AIF was translocated from mitochondria in apoptotic and necrotic OHCs. Conclusion These findings indicate that noise exposure damages DNA in the OHC, which triggers action of Caspase-3. Subsequently, AIF is translocated to the nucleus, leading to DNA damage and OHCs death.

关键词： Noise exposure Outer hair cell Single strand DNA Apoptosis induced factor Caspase.

An Overview of Electrically Evoked Otoacoustic Emissions in the Mammalian Cochlea

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Journal of Otology 2006年第1期1卷 45-50页

作者： alfred L. nuttall Oregon Hearing Research Center Department of Otolaryngology/Head & Neck SurgeryOregon Health & Science University 3181 SW Sam Jackson Park RoadNRC04 Portland Oregon 97239 USA Kresge Hearing Research Institute The University of Michigan 1301 EastAnn Street Ann Arbor Michigan 48109-0506 USA Biomedical Engineering Oregon Health & Science University 20000 NWWalker Road Beaverton OR 97006 USA Shanghai Jiao Tong University Shanghai P.R.China

Alternating currents injected into the cochlea are able to evoke outer hair cell-mediated basilar membrane motion, thus give rise to production of otoacoustic emissions. This electrically evoked otoacoustic emission(EEOAE) provides a useful tool for the research of out hair cell electromotility in vivo. This article reviews the research work on EEOAEs in mammals. Features of the EEOAEs and theories of their generation are introduced. Methods of EEOAE measurement are also described.

关键词： cochlea out hair cell electromotility otoacoustic emissions electrical stimulation

Electrically evoked auditory nerve responses in the cochlea with normal outer hair cells

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Journal of Otology 2009年第2期4卷 71-75页

作者： Josef M Miller alfred L nuttall Kresge Hearing Research Institute The University of Michigan1150 West Medical Center DriveMS IIAnn ArborMichigan 48109-0506 Oregon Hearing Research Center(NRC04) Department of Otolaryngology and Head & Neck SurgeryOregon Health Science University3181 SW Sam Jackson Park RoadPortlandOregon97239-3098

As hybrid cochlear implant devices are increasingly used for restoring hearing in patients with residual hearing, it is important to understand electrically evoked responses in cochleae having functional hair cells. To test the hypothesis that extracochlear electrical stimulation (EES) from sinusoidal current can provoke an auditory nerve response with normal frequency selectivity, the EES-evoked compound action potential(ECAP) was investigated in this study. Brief sinusoidal electrical currents, delivered via a round window electrode, were used to evoke ECAP. The ECAP waveform was observed to be the same as the acoustically evoked CAP(ACAP), except for a shorter latency. The input/output and intensity/latency functions of ACAPs and ECAPs were also similar. The maximum acoustic masking for both ACAP and ECAP occurred near probe frequencies. Since the masked tuning curve of a CAP reflects the frequency selectivity of neural excitation, these data demonstrate a highly specific activation of the auditory nerve, which would result in high degree of frequency selectivity. This frequency selectivity likely results from the cochlear traveling wave caused by electrically stimulated outer hair cells.

关键词： Gerbil Cochlea Electrical stimulation hearing cochlear implant cochlear compound action potential

MEASUREMENT OF AMPLITUDE AND DELAY OF STIMULUS FREQUENCY OTOACOUSTIC EMISSIONS

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Journal of Otology 2013年第1期8卷 57-62页

作者： Tianying Ren Jiefu Zheng Wenxuan He alfred L. nuttall Oregon Hearing Research Center Department of Otolaryngology and Head & Neck SurgeryOregon Health and Science University3181 SW Sam Jackson Park RoadPortlandOR 97239 Department of Radiology Nuclear Medicine University of Iowa Hospitals and Clinics200 Hawkins DriveIowa CityIA 52242

Although stimulus frequency otoacoustic emissions (SFOAEs) have been used as a non-invasive measure of cochlear mechanics, clinical and experimental application of SFOAEs has been limited by difficulties in accurately deriving quantitative information from sound pressure measured in the ear canal. In this study, a novel signal processing method for multicomponent analysis (MCA) was used to measure the amplitude and delay of the SFOAE. This report shows the delay-frequency distribution of the SFOAE measured from the human ear. A low level acoustical suppressor near the probe tone significantly suppressed the SFOAE, strongly indicating that the SFOAE was generated at characteristic frequency locations. Information derived from this method may reveal more details of cochlear mechanics in the human ear.

关键词： MEASUREMENT OF AMPLITUDE AND DELAY OF STIMULUS FREQUENCY OTOACOUSTIC EMISSIONS MCA SDC LDC Figure

Noise-induced nitrotyrosine increase and outer hair cell death in guinea pig cochlea

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Chinese Medical Journal 2013年第15期126卷 2923-2927页

作者： HAN Wei-ju SHI Xiao-rui alfred nuttall Chinese Peoples Liberat Army Gen Hosp Dept Otolaryngol Head & Neck Surg Beijing 100853 Peoples R China OHSU Oregon Hearing Res Ctr Portland OR USA Univ Michigan KHRI Ann Arbor MI 48109 USA

Background Modern research has provided new insights into the biological mechanisms of noise-induced hearing loss, and a number of studies showed the appearance of increased reactive oxygen species （ROS） and reactive nitrogen species （RNS） during and after noise exposure. This study was designed to investigate the noise exposure induced nitrotyrosine change and the mechanism of outer hair cells death in guinea pig cochlea. Method Thirty guinea pigs were used in this study. The experimental animals were either exposed for 4 hours per day to broadband noise at 122 dB SPL （A-weighted） for 2 consecutive days or perfused cochleae with 5 mg/ml of the SIN1 solutions, an exogenous NO and superoxide donor, for 30 minutes. Then the cochleae of the animals were dissected. Propidium iodide （PI）, a DNA intercalating fluorescent probe, was used to trace morphological changes in OHC nuclei. The distribution of nitrotyrosine （NT） in the organ of Corti and the cochlear lateral wall tissue from the guinea pigs were examined using fluorescence immunohistochemistry method. Whole mounts of organ of Corti were prepared. Morphological and fluorescent changes were examined under a confocal microscope. Results Either after noise exposure or after SIN1 perfusion, outer hair cells （OHCs） death with characteristics of both apoptotic and necrotic degradation appeared. Nitrotyrosine immunolabeling could be observed in the OHCs from the control animals. After noise exposure, NT immunostaining became much greater than the control animals in OHCs. The apoptotic OHC has significant increase of nitrotyrosine in and around the nucleus following noise exposure. In the normal later wall of cochleae, relatively weak nitrotyrosine immunolabeling could be observed. After noise exposure, nitrotyrosine immunoactivity became stronger in stria vascularis. Conclusion Noise exposure induced increase of nitrotyrosine production is associated with OHCs death suggesting reactive nitrogen species participation in th

关键词： noise exposure outer hair cell apoptosis nitrotyrosine reactive nitrogen species

噪声刺激致豚鼠外毛细胞凋亡时半胱氨酸天冬氨酸蛋白酶3激活和凋亡诱导因子转移

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中华耳鼻咽喉头颈外科杂志 2007年第7期42卷 515-519页

作者：韩维举史晓瑞 alfred nuttall 解放军总医院耳鼻咽喉头颈外科北京100853 Oregon Hearing Research Center Oregon Health and Science University USA Kresge Hearing Research Institute The University of Michigan USA

目的探讨噪声损伤后豚鼠外毛细胞发生凋亡的通路及其机制。方法分离解剖对照组(12只)和噪声暴露组(12只)豚鼠耳蜗,利用免疫荧光抗体和免疫荧光染料,分别染色细胞核、线粒体、凋亡诱导因子(apoptosis inducing factor,AIF)和半胱氨酸天... 详细信息

目的探讨噪声损伤后豚鼠外毛细胞发生凋亡的通路及其机制。方法分离解剖对照组(12只)和噪声暴露组(12只)豚鼠耳蜗,利用免疫荧光抗体和免疫荧光染料,分别染色细胞核、线粒体、凋亡诱导因子(apoptosis inducing factor,AIF)和半胱氨酸天冬氨酸蛋白酶3(Caspase 3),按表面制备法行耳蜗铺片,观察凋亡和坏死毛细胞内的荧光信号。结果对照组正常耳蜗毛细胞内没有激活的 Caspase 3,AIF 分布在毛细胞的线粒体内。实验组动物暴露于声压级120 dB 的白噪声环境中每天4 h,连续2 d 后,耳蜗外毛细胞出现死亡,表现为坏死和凋亡两种方式,但以凋亡为主。在凋亡的外毛细胞中,Caspase 3被激活,AIF 从线粒体转移到细胞核中;而在坏死的外毛细胞中,没有 Caspase3的激活,只有 AIF 自线粒体向细胞核的转移。结论噪声损伤后耳蜗外毛细胞的凋亡以 Caspase 依赖型的通路为主;线粒体释放的 AIF 在外毛细胞死亡通路中起重要作用。

关键词：噪声毛细胞,外细胞凋亡凋亡诱导因子半胱氨酸天冬氨酸蛋白酶3

Direct current pulse elicits basilar membrane vibration in guinea pigs

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Journal of Medical Colleges of PLA(China) 2000年第3期15卷 231-235页

作者：郭梦和任田英 alfred L nuttall

Objective:To study the electromotility of the basilar membrane (BM) of guinea pigs in vivo. Methods :A pair of platinum-iridium wire electrodes were deposited into the holes drilled into the scala vestibuli and scala tympani on the basal turn of cochlea. The organ of Corti was stimulated with rectangular, constant current pulses . The displacement and velocity of BM were measured with laser doppler velocimeter. Results: The electrically elicited displacement of BM moved toward the scala where the electrode was positively charged. The waveform of BM displacement generally corresponded to the shape of the rectangular pulse of electric current. Ringing responses could be seen at the onset and offset of current pulse reflecting transient responses of the organ of Corti. In the cochlea of hearing-impaired or dead animal, direct current (DC) could still elicit a BM displacement but the ringing response was attenuated or disappeared. This phenomenon was probably due to metabolic disturbance in the damaged outer hair cells. In the sensitive cochlea, the BM vibration induced with direct current was similar to that induced by acoustic stimulation, and the BM moves in a traveling wave pattern. Conclusion: The findings of this experiment implicated that the DC stimulation of the cochlea conduces the contraction or elongation of OHCs. The electromotility of OHCs provides sufficient force to displace the BM. In the electrically stimulated normal cochlea,transient response of OHCs can induce resonant vibration at the same frequency as that Of the characteristic frequency (CF) of a partition in the BM. The vibration should be an active process of energy depletion associated with the cochlear *** vibration of BM can propagate to other partition of BM according to the traveling wave theory. This characteristic has laid the foundation for the electromotile hearing and electrically evoked otoacoustic emission.

关键词： cochlea vibration basilar membrane electromotility

噪声损伤引起耳蜗外毛细胞凋亡时细胞核内单链DNA的产生及EndoG的转移

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中华耳科学杂志 2008年第2期6卷 209-215页

作者：韩维举史晓瑞 alfred nuttall 解放军总医院耳鼻咽喉头颈外科北京100853 俄勒冈医科大学听力研究中心

目的观察噪声损伤后耳蜗外毛细胞内单链DNA和EndoG的变化,探讨耳蜗外毛细胞的死亡机制。方法豚鼠随机分为噪声暴露组、MNNG耳蜗灌流组和对照组(每组各12只);小鼠随机分为噪声暴露组和对照组(每组12只)。分离解剖耳蜗后,用碘化丙啶(PI)... 详细信息

目的观察噪声损伤后耳蜗外毛细胞内单链DNA和EndoG的变化,探讨耳蜗外毛细胞的死亡机制。方法豚鼠随机分为噪声暴露组、MNNG耳蜗灌流组和对照组(每组各12只);小鼠随机分为噪声暴露组和对照组(每组12只)。分离解剖耳蜗后,用碘化丙啶(PI)染色细胞核、Pholloidin染色F-actin,免疫荧光抗体分别染色单链DNA(ssDNA)、核酸内切酶G(Endonuclease G EndoG)和凋亡诱导因子(Apoptosis inducing factors,AIF),制备耳蜗铺片,激光共聚焦显微镜下观察凋亡和坏死毛细胞内的荧光信号变化。结果(1)暴露于120dBSPL的白噪声环境中每天4小时,连续2天后引起豚鼠和小鼠耳蜗外毛细胞凋亡时,其细胞核内产生ssDNA,而在正常细胞内没有三ssDNA;(2)在正常情况下,EndoG分布于耳蜗毛细胞的细胞核外,在暴露于上述噪声后发生凋亡和坏死的豚鼠耳蜗外毛细胞中,EndoG从细胞核外转移到细胞核内,细胞核中的EndoG显著增加;(3)豚鼠耳蜗外淋巴灌流烷化剂MNNG后发生耳蜗外毛细胞凋亡和坏死,在凋亡和坏死的耳蜗外毛细胞中,AIF自线粒体转移到细胞核,其变化与噪声损伤引起耳蜗外毛细胞凋亡和坏死时一致。结论噪声刺激或烷化剂MNNG灌流后,造成耳蜗外毛细胞DNA损伤,产生ssDNA,引起AIF和EndoG自线粒体释放,激活Caspase-3,AIF和EndoG进一步向细胞核转移,最终使细胞核内的DNA降解,导致耳蜗毛细胞的死亡。

关键词：噪声外毛细胞凋亡诱导因子单链DNA 核酸内切酶G

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乙酰胆碱对豚鼠SMA平滑肌细胞的作用

农垦医学 2004年第3期26卷 163-165页

作者：张春军范平司军强孙志萍蒋志根 alfred L.nuttall 石河子大学医学院 Oregon Hearing Research Center Oregon Health&Science UniversityPortland.OR 97201USA Oregon

耳蜗血流障碍与听力丧失有着密切联系[1～4].乙酰胆碱(Ach)作为一种神经递质和血管舒张物质参与了许多血管床的调节活动[5～10].实验已证实,在大鼠和猫的脑血管床有大量的胆碱乙酰化酶免疫反应阳性的神经纤维[8];Ach和它的模拟剂能引起... 详细信息

耳蜗血流障碍与听力丧失有着密切联系[1～4].乙酰胆碱(Ach)作为一种神经递质和血管舒张物质参与了许多血管床的调节活动[5～10].实验已证实,在大鼠和猫的脑血管床有大量的胆碱乙酰化酶免疫反应阳性的神经纤维[8];Ach和它的模拟剂能引起内耳螺旋动脉(spiral modiolar artery,SMA)的舒张,并且蕈毒碱的拮抗剂能减少耳蜗血流[5](cochlea blood flow,CBF),这些结果均说明胆碱能的神经纤维参与了内耳的微循环调节.

关键词：乙酰胆碱豚鼠 SMA 平滑肌细胞内耳螺旋动脉