Auditory brainstem volume-conducted responses: origins in the laboratory mouse.

K R Henry
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Abstract

Volume-conducted, short-latency auditory-evoked potentials were examined in the laboratory mouse with lesions and local recording used to localize their sources. PI corresponds in time with N1 recorded from the round window, while isolation of the eighth cranial nerve from the brainstem results in the loss of all post-PI components. PII latency agrees with that of evoked potentials recorded from the cochlear nucleus. PIII latency corresponds with that of evoked potentials from the vicinity of the contralateral superior olivary nucleus, and lesions of this and closely related contralateral structures abolish PIII from the vertex recordings. PIV is reduced in amplitude by unilateral brainstem lesions between the superior olive and the inferior colliculus. Evoked potentials and lesions localized PV to the vicinity of the lateral regions of the contralateral inferior colliculus. PVI disappeared when areas anterior to the inferior colliculi were lesioned. Although minor species differences may exist, it was concluded that the sources for PI to V in the mouse closely resemble those in the cat, and they agree well with the limited data from the human. This technique may now be applied to studies of the numerous auditory mutants of the laboratory mouse.

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听觉脑干体积传导反应:实验小鼠的起源。
在有损伤的实验室小鼠中检测了体积传导的短潜伏期听觉诱发电位,并使用局部记录来定位其来源。PI与圆窗记录的N1在时间上对应,而从脑干分离第八脑神经导致PI后组分全部丢失。PII潜伏期与耳蜗核记录的诱发电位一致。PIII潜伏期与对侧橄榄上核附近的诱发电位相对应,对侧橄榄上核及密切相关的对侧结构病变使PIII从顶点记录中消失。PIV在上橄榄和下丘之间的单侧脑干病变时振幅降低。诱发电位和病变将PV定位于对侧下丘外侧区域附近。下丘前部病变时PVI消失。虽然可能存在微小的物种差异,但得出的结论是,小鼠中PI到V的来源与猫中的来源非常相似,并且与人类的有限数据非常吻合。这项技术现在可以应用于研究实验室小鼠的许多听觉突变体。
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