Tinnitus Correlates with Downregulation of Cortical Glutamate Decarboxylase 65 Expression But Not Auditory Cortical Map Reorganization
Tinnitus Correlates with Downregulation of Cortical Glutamate Decarboxylase 65 Expression But Not Auditory Cortical Map Reorganization
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DOI：
10.1523/jneurosci.1117-19.2019
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发表时间：
2019-12-11
影响因子：
5.3
通讯作者：
Bao, Shaowen
中科院分区：
文献类型：
--
作者：
Miyakawa, Asako;Wang, Weihua;Bao, Shaowen
听力损失是耳鸣的最大危险因素，听力损失相关的听觉通路的病理变化已被假设为耳鸣的潜在机制。耳鸣是听力损失的一种表现，也是听力损失的一种表现。在这项研究中，我们分离耳鸣和听力损失的FVB小鼠，表现出强大的阻力耳鸣单耳噪声引起的听力损失。此外，敲低谷氨酸脱羧酶65（GAD 65）的表达在听觉皮层（AI）的RNA干扰引起耳鸣听力正常的FVB小鼠。我们发现耳鸣与AI中GAD 65的下调显著相关。相比之下，皮质地图失真，这已被假设为耳鸣的机制，与听力损失，但耳鸣无关。我们的研究结果为耳鸣和其他幻痛的康复提供了新的策略。
Hearing loss is the biggest risk factor for tinnitus, and hearing-loss-related pathological changes in the auditory pathway have been hypothesized as the mechanism underlying tinnitus. However, due to the comorbidity of tinnitus and hearing loss, it has been difficult to differentiate between neural correlates of tinnitus and consequences of hearing loss. In this study, we dissociated tinnitus and hearing loss in FVB mice, which exhibit robust resistance to tinnitus following monaural noise-induced hearing loss. Furthermore, knock-down of glutamate decarboxylase 65 (GAD65) expression in auditory cortex (AI) by RNA interference gave rise to tinnitus in normal-hearing FVB mice. We found that tinnitus was significantly correlated with downregulation of GAD65 in the AI. By contrast, cortical map distortions, which have been hypothesized as a mechanism underlying tinnitus, were correlated with hearing loss but not tinnitus. Our findings suggest new strategies for the rehabilitation of tinnitus and other phantom sensation, such as phantom pain.