Kusakari J, Arakawa E, Rokugo M, Ohyama K, Inamura N
Laryngoscope. 1984 Oct;94(10):1365-9. doi: 10.1288/00005537-198410000-00019.
Although the N1 latency of whole nerve action potential is one of the important pieces of information obtained from ECochG, there are some conflicting opinions as to whether or not it is prolonged in sensorineural hearing loss. Kainic acid (KA) is known to destroy neurons selectively through an action at glutamatergic synapses. Therefore, a model of "neural deafness" was made by perfusing the scala tympani with KA solution. The effect of KA upon cochlear microphonics was minimal. Although the N1 amplitude was markedly suppressed by KA, the N1 latency was neither prolonged nor shortened. The result obtained in the present study strongly suggests that the N1 latency is not prolonged in "neural deafness."
虽然全神经动作电位的N1潜伏期是从耳蜗电图获得的重要信息之一，但关于它在感音神经性听力损失中是否延长存在一些相互矛盾的观点。已知 kainic 酸（KA）通过作用于谷氨酸能突触选择性地破坏神经元。因此，通过向鼓阶灌注KA溶液建立了“神经性耳聋”模型。KA对耳蜗微音器电位的影响最小。虽然KA明显抑制了N1波幅，但N1潜伏期既未延长也未缩短。本研究获得的结果有力地表明，“神经性耳聋”中N1潜伏期并未延长。
