Whole-nerve Action Potential Research Articles

Relations among Behavioral Thresholds, Cochlear Potentials, and Cochlear Injury following Traumatic Exposures to a Wide-Band Noise in the Chinchilla

Four monaural chinchillas were exposed to white noise (0.25–10 kHz) at 108 dB SPL for 220 min. Behavioral thresholds were measured subsequently for three months. Permanent threshold shifts of about 60 dB were observed for frequencies above 1400 Hz and of about 10 dB for frequencies below 1000 Hz. Cochlear microphonics were measured differentially. In the three turns of the cochlea, the respective losses of sensitivity were more than 60, 30–60, and 15–50 dB. The losses of maximum available microphonic voltage were more than 40, 25–30, and 10–20 dB, respectively. The whole-nerve action potential in response to clicks contained no component that could be masked by high-frequency noise and is attributed only to more-apical parts of the cochlea. Hair cells were entirely or almost completely absent in the basal turn, markedly reduced in the second turn, and nearly normal in the third turn. Corresponding losses of neurons were observed at the different levels of the spiral ganglion. [Work supported by National Institutes of Health, Public Health Service, U. S. Department of Health, Education, and Welfare.]

Analyses of Auditory-Nerve Action Potentials in the Chinchilla

Teas, Eldredge, and Davis [J. Acoust. Soc. Am. 34, 1438–1459 (1962)] proposed a model for the physiological and electrical properties of whole-nerve action potentials recorded with cochlear electrodes in the guinea pig. Action potentials for clicks were differentially disrupted by bands of noise with constant spectrum level as the high-pass frequency of the noise was lowered. The incremental changes in waveform resembled action-potential waveforms occurring at successively later times and corresponding to known traveling-wave delays. The model was supported by the changes observed following localized chemical injuries in the cochlea and by the ability of the model to predict the waveform elicited by bursts of high-frequency tones. The method has been applied to the chinchilla in an improved form with a LINC computer. Similar relations are observed and further support for the model is found in the altered relations associated with anatomically verified lesions of the cochlea. [Work supported by National Institutes of Health, Public Health Service, U. S. Department of Health, Education, and Welfare.]

Auditory Nerve Responses to Low-Pass Transients

Masking has been used to subtract groups of nerve impulses from the whole-nerve action potential of the guinea pig. The form of that part of the whole-nerve action potential which is eliminated by a narrow band of noise is approximately diphasic. This is the expected form of individual nerve impulses recorded from one electrode in the cochlea and the other on the neck. The stimulus variables investigated were intensity and rise time of the acoustic transient, and intensity, bandwidth, and center frequency of the masking noise. The whole-nerve action potential to low-pass transients is composed of impulses that arise from a large extent of the organ of Corti, with a distribution in time that parallels the space-time pattern of the cochlear microphonic. (This research was supported by Bt-366-C2 and NIH-B1726.)

Latency of Action Potentials in the Cochlea of the Guinea Pig

The latency of the well-synchronized whole-nerve action potential (AP) in the cochlea of the guinea pig includes both neural and traveling-wave delays. The latency varies with the intensity and with the frequency of the acoustic stimulus. Selective local interference with the response was produced by (1) selective masking, (2) local fatigue of sensory elements, and (3) local injection of drugs. Such interference the basal turn prolonged the latency of the AP response. Low-frequency tones can reduce the N1 response to click stimuli without changing the modal latency. Apparently nearly all of the well-synchronized AP is due to neurons that arise in the first turn of the cochlea, regardless of the frequency of stimulation. The traveling-wave delay appears as a significant component of latency only in the smaller AP responses that remain after the impulses arising in the first turn are suppressed. Information about the time of onset of an acoustic signal can be delivered to the central nervous system primarily by the best-synchronized or modal portion of the AP response.

Latency of Action Potentials in the Cochlea of Guinea Pig

The latency of the well-synchronized whole-nerve action potential (AP) in the cochlea of the guinea pig includes both neural and traveling-wave delays. The latency varies with the intensity and with the frequency of the acoustic stimulus. Selective local interference with the response was produced by (1) selective masking, (2) local fatigue of sensory elements, and (3) local injection of drugs. Such interference in the basal turn prolonged the latency of the AP response. Interference in higher turns suppressed later portions of the response without changing the modal latency. Apparently nearly all of the well-synchronized AP is due to neurons that arise in the first turn of the cochlea, regardless of the frequency of stimulation. The traveling wave delay appears as a component of latency only in the smaller AP responses that remain after the impulses arising in the first turn are suppressed. Apparently information about the time of onset of an acoustic signal is delivered to the central nervous system primarily by the well-synchronized initial portion of the AP response. (Supported by the Office of Naval Research, Contract N6onr 272.)