卡铂-南美栗鼠听觉神经病模型中的同步听神经活动。
Synchronous auditory nerve activity in the carboplatin-chinchilla model of auditory neuropathy.
机构信息
Department of Psychology, Dalhousie University, 1355 Oxford Street, Halifax, Nova Scotia B3H 4J1, Canada.
出版信息
J Acoust Soc Am. 2010 Jul;128(1):EL56-62. doi: 10.1121/1.3453764.
Abstract
Two hallmark features of auditory neuropathy (AN) are normal outer hair cell function in the presence of an absent/abnormal auditory brainstem response (ABR). Studies of human AN patients are unable to determine whether disruption of the ABR is the result of a reduction of neural input, a loss of auditory nerve fiber (ANF) synchrony, or both. Neurophysiological data from the carboplatin model of AN reveal intact neural synchrony in the auditory nerve and inferior colliculus, despite significant reductions in neural input. These data suggest that (1), intact neural synchrony is available to support an ABR following carboplatin treatment and, (2), impaired spike timing intrinsic to neurons is required for the disruption of the ABR observed in human AN.
摘要
听觉神经病 (AN) 的两个显著特征是在外毛细胞功能正常的情况下，听觉脑干反应 (ABR) 缺失/异常。对人类 AN 患者的研究无法确定 ABR 的中断是由于神经输入减少、听神经纤维 (ANF) 同步性丧失还是两者兼而有之。来自卡铂诱导的 AN 模型的神经生理学数据显示，尽管神经输入显著减少，但听觉神经和下丘中的神经同步仍然完整。这些数据表明：(1) 卡铂处理后仍可利用完整的神经同步来支持 ABR；(2) 人类 AN 中观察到的 ABR 中断需要神经元内在的受损的尖峰定时。
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