Origin of AP in electrocochleogram as ivestigated by microelectrode technique

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Compound AP evoked by electrical stimuli (EAP) applied to the cochlea in guinea pigs were recorded in the auditory nerve trunk to know origin of compound ap by acoustic stimuli. EAP consisted of a few negative potentials. In normal cochleas the amplitude of the first negative potential (N1 potential) with latency of less 1 msec rapidly grew and its dynaimic range was 6 dB. In cochleas damaged with kanamycin s.c., the growth response of the N1 potential was the same as that in normal cochleas. This showed that the N1 potential originated from potential of cochlear nerve stimulated by electrical current. As far as threshold with respect to stimulus intensity is concerned, there is a difference to acoustic stimulation. With electrical stimulation the lower the stimulus frequency was, the lower the threshold of the N1 potential was.The latency of the second negative potential (N2 potential) for electrical stimulation was between 1 and 2 msec depending on stimulus strength. In normal cochleas the amplitude of the N2 potential grew slowly. In cochleas damaged with kanamycin the linear growth response of the amplitude was lost. From these findings N2 potential was identified as electrophonic effect in origin.Since the N1 potential evoked by acoustic stimulation shows sensitivities of both hair cells and cochlear nerve, the potential always doesn't show the sensitivity of cochlear nerve. Using round-window stimulation in normally hearing guinea pigs, it was shown that intravenously injected Lidocaine and Aspirin decreased the sensitivities of cochlear nerve fibres in addition to hair cells.