Abstract
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."
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