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J Assoc Res Otolaryngol. 2005 Mar;6(1):48-62. doi: 10.1007/s10162-004-5009-2. Epub 2005 Apr 22.
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本文引用的文献

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Efferent-mediated adaptation of the DPOAE as a predictor of aminoglycoside toxicity.作为氨基糖苷类毒性预测指标的传出神经介导的畸变产物耳声发射适应性
Hear Res. 2005 Mar;201(1-2):99-108. doi: 10.1016/j.heares.2004.09.010.
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Chronic excitotoxicity in the guinea pig cochlea induces temporary functional deficits without disrupting otoacoustic emissions.豚鼠耳蜗中的慢性兴奋毒性会诱发暂时性功能缺陷,而不会干扰耳声发射。
J Acoust Soc Am. 2004 Aug;116(2):1044-56. doi: 10.1121/1.1772395.
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The distribution and the modulation of tyrosine hydroxylase immunoreactivity in the lateral olivocochlear system of the guinea-pig.
Neuroscience. 2004;125(3):725-33. doi: 10.1016/j.neuroscience.2004.02.023.
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Transient focal cooling at the round window and cochlear nucleus shows round window CAP originates from cochlear neurones alone.圆窗和蜗神经核处的短暂局灶性冷却表明,圆窗复合动作电位仅起源于耳蜗神经元。
Hear Res. 2004 Apr;190(1-2):75-86. doi: 10.1016/S0378-5955(03)00403-9.
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Dopaminergic olivocochlear neurons originate in the high frequency region of the lateral superior olive of guinea pigs.
Hear Res. 2004 Jan;187(1-2):122-30. doi: 10.1016/s0378-5955(03)00308-3.
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Modulation of cochlear afferent response by the lateral olivocochlear system: activation via electrical stimulation of the inferior colliculus.外侧橄榄耳蜗系统对耳蜗传入反应的调制:通过下丘电刺激实现激活
J Neurophysiol. 2003 Nov;90(5):3178-200. doi: 10.1152/jn.00537.2003.
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Real-time quantitative RT-PCR for low-abundance transcripts in the inner ear: analysis of neurotrophic factor expression.内耳低丰度转录本的实时定量逆转录聚合酶链反应:神经营养因子表达分析
Hear Res. 2003 Nov;185(1-2):97-108. doi: 10.1016/s0378-5955(03)00298-3.
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Anatomy of olivocochlear neurons in the hamster studied with FluoroGold.
Hear Res. 2003 Nov;185(1-2):65-76. doi: 10.1016/s0378-5955(03)00213-2.
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Pathways for protection from noise induced hearing loss.
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Diversity of axonal ramifications belonging to single lateral and medial olivocochlear neurons.属于单个外侧和内侧橄榄耳蜗神经元的轴突分支的多样性。
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通过多巴胺能神经毒素破坏外侧橄榄耳蜗神经元会抑制声音诱发的听神经活动。

Disruption of lateral olivocochlear neurons via a dopaminergic neurotoxin depresses sound-evoked auditory nerve activity.

作者信息

Le Prell Colleen G, Halsey Kärin, Hughes Larry F, Dolan David F, Bledsoe Sanford C

机构信息

Kresge Hearing Research Institute, University of Michigan Medical School, Ann Arbor, MI 48109-0506, USA.

出版信息

J Assoc Res Otolaryngol. 2005 Mar;6(1):48-62. doi: 10.1007/s10162-004-5009-2. Epub 2005 Apr 22.

DOI:10.1007/s10162-004-5009-2
PMID:15735934
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2504639/
Abstract

We applied the dopaminergic (DA) neurotoxin 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) to the guinea pig cochlear perilymph. Immunolabeling of lateral olivocochlear (LOC) neurons using antibodies against synaptophysin was reduced after the MPTP treatment. In contrast, labeling of the medial olivocochlear innervation remained intact. As after brainstem lesions of the lateral superior olive (LSO), the site of origin of the LOC neurons, the main effect of disrupting LOC innervation of the cochlea via MPTP was a depression of the amplitude of the compound action potential (CAP). CAP amplitude depression was similar to that produced by LSO lesions. Latency of the N1 component of the CAP, and distortion product otoacoustic emission amplitude and adaptation were unchanged by the MPTP treatment. This technique for selectively lesioning descending LOC efferents provides a new opportunity for examining LOC modulation of afferent activity and behavioral measures of perception.

摘要

我们将多巴胺能(DA)神经毒素1-甲基-4-苯基-1,2,3,6-四氢吡啶(MPTP)应用于豚鼠耳蜗外淋巴。使用抗突触素抗体对外侧橄榄耳蜗(LOC)神经元进行免疫标记,在MPTP处理后减少。相比之下,内侧橄榄耳蜗神经支配的标记保持完整。正如外侧上橄榄核(LSO)——LOC神经元的起源部位——发生脑干损伤后一样,通过MPTP破坏耳蜗的LOC神经支配的主要作用是复合动作电位(CAP)幅度降低。CAP幅度降低与LSO损伤所产生的情况相似。MPTP处理并未改变CAP的N1成分的潜伏期、畸变产物耳声发射幅度及适应性。这种选择性损伤下行LOC传出纤维的技术为研究LOC对传入活动的调节及行为感知测量提供了新机会。