Short latency auditory evoked brain-stem potentials in response to monaural click stimuli were topographically recorded on the skull of the dogs with a no-cephlic reference. Five scalp positive potentials (P1, 2, …5) were identified before a deep through and one or two positive potentials followed it. P1 was positive in polarity at the contralateral ear and the vertex, and negative in polarity at the ipsilateral ear with the greatest negativity in the vicinity of the tympanic bulla. It was suggested that the cochlea and the cochlear nerve are the possible generators for this component. P2 was positive in polarity with its maximal amplitude at the base of the ipsilateral pinna. The significant latency difference according to electrode positions was not elicited for this component. P3 was negative in the vicinity of the stimulated ear and positive in polarity at other recording positions. This polarity reversal of the third wave is also pointed out in man and cat. Double-peaked P3 was occasionally recorded in the dog as noted in the monkey. P4 was positive at all electrode positions and its amplitude was slightly lateralied to the contralateral side. Its latency shift was not significant. P5 was maximal in the midsagittal plane without lateral amplitude asymmetry. Its latency was latest at the vertex. It was concluded that there was significant disparity in potential field distributions among different animal species, so it is necessary to bear in mind these differences in comparing the data obtained from various animals. The ABR of the dog by bipolar recording, which is equivalent to the vertex-earlobe diagonal array in humans, consisted of four waves before the deep through, in stead of five wares by monopolar recording. This is due to the fact that P2 by monopolar recording was absorbed into the negative through between the first and second wave by bipolar recording. The dog is one of the useful experimental materials for audiological researches because the temporo-spatial distribution of the ABR of the dog is more akin to that of humans than other small animals.
In order to investigate the relationship between renal failure and hearing loss, we made the guinea pigs with renal failure which was experimentally induced and examined the cochlear potentials (AP, CM and EP). As the renal damage was higher, the amplitude of AP and CM were decreased and the latency of AP was prolonged. But EP was within normal range. It was thought that the sensory cells of the cochlea was responsible for hearing loss of the guinea pigs with renal failure. No pathological findings of the cochlea was found under a light microscope, and it was suggested that the etiology of hearing loss was mainly metabolic disturbances such as uremic toxicities, electrolyte imbalance and endocrine abnormalities.
This preliminary experiment is concerned with the frequency distribution of two-tone suppression. The first masker M1 (suppressee) was a narrowband noise centered and fixed at 3kHz (F1) with 200Hz bandwidth and spectrum level -10-30dB in SPL, the second masker M2 (suppressor), also was a narrow-band noise with 200Hz bandwidth and spectrum level -15-40dB in SPL. Levels of the stimulus components (suppressee and suppressor) were the experimental parameters. In all experiments the threshold of a 15ms probe tone (fixed at 3kHz) following a 600ms M1 was determined as a function of central frequency (F2) of a 600ms M2. The suppressor central frequency F2 ranged from 1.4 to 6kHz. At appropriate levels and frequencies all subjects showed significant suppression both for F2>F1 and for F2<F1. For F2<F1 than for F2>F1, however, suppression was more prominent. Also, suppression occured at higher suppressee level than at lower suppressor levl for F2>F1 at appropriate suppressor levels and suppressee levels. Suppression was found to decrease to zero as F2 approached F1. Suppression showed at the suppressor frequencies ranging from just above or below the critical band of F1 to well beyound the 2-3 critical bands. The amount of suppression depended on both suppressor level and suppressee level in a way accounted for the Duifhuis' model of two-tone suppression. For spectrum levels of suppressor as low as 40dB in SPL, the effect of levels on suppression was linear, i.e., suppression magnitude was seen to be a monotonically increasing function. These results have demonstrated effects similar to two-tone suppression in auditory-nerve fibers in psychophysical experiments in humans. In most of the psychophysical experiments, however, signal frequency has been equal to masker frequency. Thus, there is little information about the frequency distribution of suppression effects. This is main factor investigated in the next papers.
These experiments are concerned with the frequency distribution of two-tone suppression in forward masking. In each experiment the threshold of a 15ms probe tone following a 600ms narrow-band noise masker was determined as a function of probe frequency. Probe threshold was measured for a fixed narrow-band noise centered at 3kHz with 200Hz bandwidth and spectrum level of 20dB in SPL with and without a suppressing narrow-band noise with 200Hz bandwidth and spectrum level of 40dB in SPL whose central frequency was systematically varied. The suppression, measured as a reduction in probe threshold produced by adding the suppressing narrow-band noise, was found to have three components. First, frequency distribution of suppression was limited to a narrow range of probe frequencies around 3kHz and does not reflect a simple reduction in the level of suppression noise, i.e., part of the suppression can be attributed to reduction of the effective level of the suppressed noise in a particular region. Second, for central frequency (F2) of the suppressing noise below central frequency (F1) of the suppressed noise, the suppressed frequency region lies around 0.6 to 0.85F1 and F2 above F1 the suppressed frequency region lies around 1.30t 1.9F1. However, they are in disagreement with the notion proposed by Javel et al. (1978) that suppression magnitude is related to the frequency difference between the travelling wave peaks for F2 and F1 on the basilar membrane. Third, these data indicated that there is much more suppression for F2<F1 than F2>F1. This effect can be explained with the help of the Hall's nonlinear model on the basiler membrane. These data are in general agreement with previously published reports of physiological suppression behavior, and they support the concept that the suppression is generated primarily as a result of interactions occurring within hair cells or stereo-ciliary-tectrial structures.