Tinnitus: animal models and findings in humans.

Tinnitus: animal models and findings in humans.
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DOI:
10.1007/s00441-014-1992-8
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发表时间:
2015-07
影响因子:
3.6
通讯作者:
Roberts, Larry E.
Roberts, Larry E.
中科院分区:
生物学3区
文献类型:
--
作者:
Eggermont, Jos J.;Roberts, Larry E.

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慢性耳鸣(耳鸣)是一种医学上无法治愈的疾病,会降低全球数百万人的生活质量。大多数病例与听力损失有关,听力损失可以通过听力图或更敏感的方法检测到。来自动物模型和对人类耳鸣患者的研究的汇聚证据表明,虽然耳蜗损伤是触发因素,但大多数耳鸣病例并不是由持续在耳蜗处的刺激性过程产生的,而是由于当听觉神经元失去来自耳朵的输入时,中枢听觉通路发生的变化。神经可塑性的形式是这些神经变化的基础,包括去传入中枢听觉结构中自发活动和神经获得的增加,这些结构中的同步活动增加,听觉皮质的紧张性组织的改变,以及通过耳鸣患者的功能成像发现并经动物研究证实的非听觉脑区网络行为的改变。耳鸣神经改变的分子机制研究还处于初级阶段,是研究的前沿。
Chronic tinnitus (ringing of the ears) is a medically untreatable condition that reduces quality of life for millions of individuals worldwide. Most cases are associated with hearing loss that may be detected by the audiogram or by more sensitive measures. Converging evidence from animal models and studies of human tinnitus sufferers indicates that, while cochlear damage is a trigger, most cases of tinnitus are not generated by irritative processes persisting in the cochlea but by changes that take place in central auditory pathways when auditory neurons lose their input from the ear. Forms of neural plasticity underlie these neural changes, which include increased spontaneous activity and neural gain in deafferented central auditory structures, increased synchronous activity in these structures, alterations in the tonotopic organization of auditory cortex, and changes in network behavior in nonauditory brain regions detected by functional imaging of individuals with tinnitus and corroborated by animal investigations. Research on the molecular mechanisms that underlie neural changes in tinnitus is in its infancy and represents a frontier for investigation.
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