[A modified template for charting auditory threshold levels on audiograms in normal age-related hearing changes and presbycusis praecox].
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Absolute thresholds from 125 Hz to 52 kHz are determined for six guinea pigs trained by a positive reinforcement method. Four to five hundred trials were conducted during daily testing sessions and little between- or within-subject variability was found. Two of the six animals were subsequently treated with kanamycin and the development of a hearing loss for the high frequencies was followed. Loss of outer and to a lesser extent inner hair cells was well correlated with the threshold shift observed. Contrary to the experience of previous investigators, this operant training procedure has proved as efficient as that for other species of experimental animals, such as the monkey and the chinchilla. It holds excellent promise for future auditory behavioral work with the guinea pig.
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A derived response method of acquiring frequency specific auditory evoked potentials that utilizes a pure tone in combination with a toneburst is applied to the measurement of hearing sensitivity in guinea pigs, chinchillas and pocket gophers. Two experiments which demonstrate that thresholds acquired via tone-derived responses are 10 to 15 dB more sensitive than thresholds to solitary tonebursts are described. The derived potentials approximate behaviorally acquired thresholds at frequencies of 0.5 kHz and above. This technique may provide a more rapid means of assessing hearing sensitivity in laboratory animals than by behavioral means.
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The density of cochlear inner hair cells in Wistar rats is greatest on a short section of the basilar membrane about a fifth of its length from the base. This place corresponds to the frequency region of 30--40 kHz which is supposed to be the region of best hearing.
Hypoxia has long been hypothesized to play a role in noise-induced hearing loss, and the disruption of auditory function by asphyxiation has been repeatedly demonstrated. Recent data, however, suggest that the cochlea is resistant to less extreme hypoxic events. The current report describes the combined effects of noise and hypoxia on a measure of auditory function, in an effort to clarify the role of hypoxia in hearing loss. Exposure to 1200 parts per million of carbon monoxide in air for 90 min preceding and 120 min concurrent with exposure to a broad-band noise at 110 dBA produced high-frequency threshold shifts of greater magnitude than those produced by exposure to noise alone. An equivalent carbon monoxide exposure in a 'quiet' environment did not produce any change in auditory detection thresholds. The potentiation of noise-induced threshold shifts by carbon monoxide provides additional support for the hypothesized role of metabolic exhaustion or bloodflow impairment in noise-induced hearing loss. It also suggests a possible interpretation of clinical findings of auditory impairment associated with carbon monoxide exposure.
The inner ear sometimes acts as a robust sound generator, continuously broadcasting sounds (spontaneous otoacoustic emissions) which can be intense enough to be heard by other individuals standing nearby. Paradoxically, most individuals are unaware of the sounds generated within their ears. Two hypotheses could explain this paradox: (1) the spontaneous emissions may not be transmitted to the central nervous system; or (2) the spontaneous emission produces a continuous, high rate of neural activity, which, like the natural pattern of spontaneous activity, is ignored by the central nervous system. Here we demonstrate that high-intensity spontaneous otoacoustic emission can vigorously activate auditory nerve fibres in mammals (Chinchilla laniger). This 'internal biological noise' creates a 'line busy' signal that significantly degrades a neuron's ability to respond to sound and results in a hearing loss completely different from that caused by damage to sensory cells.
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