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Innate susceptibility to audiogenic seizures develops and declines at varying rates and ages, depending upon genotype and environmental conditions. Auditory dysfunctions have been experimentally produced which induce susceptibility in otherwise nonsusceptible mouse strains. In order to more closely correlate cochlear functions and audiogenic seizures in genetically susceptible mice, both measures were obtained from LP/J mice, at ages ranging from 8 to 120 days. Susceptibility to sound-produced convulsions was first noted at 12 days, was maximal from 18 to 32 days, declined rapidly by 40 days, and disappeared by 120 days of age. Cochlear nerve-evoked potential thresholds were very high at 12 days, were lowest between 18 and 32 days and increased thereafter. The correlation between susceptibility and cochlear thresholds was greatest for high frequencies (r = -.93), intermediate for midfrequency (r = -.77), and poorest for low frequencies (r = -.56). It was concluded that either genetic or environmental factors which produce an intermediate level of high frequency cochlear damage in the young mouse will produce susceptibility to audiogenetic seizures. [ABSTRACT FROM AUTHOR]

A technique is described that can nontraumatically assess cochlear microphonic (CM) and cochlear action potential (AP) thresholds to pure tones in the intact mouse. This method was applied to the normal hearing CBA/J, and to the C57BL/6J, which has early-onset hearing loss. CM thresholds axe most sensitive m both mice by 23 days of age, and the C57BL/6J CM responses degenerate rapidly thereafter, especially at the high-frequency end. The CMs of the CBA/J continue to change past 23 days, developing a threshold dip at 24 kHz, and becoming slightly less sensitive at 32 kHz. The AP of the C57BL/6J is also most sensitive at 23 days, and becomes gradually less sensitive to 32- and 64-kHz tones over the next 36 days. The CBA/J AP thresholds are not maximally sensitive until 41 days of age. [ABSTRACT FROM AUTHOR]

The vertex-positive, volume-conducted far field response was used to evaluate age-related changes of the 8th cranial nerve and auditory brainstem in the anesthetized C57BL/6 mouse. Responses were obtained from stimuli as low as 10 dB (within the 10-20 kHz bandpass). When latencies were compared between 16- and 35-day-old subjects, the older mice had a P1 component which was .175 msec faster, a P2 which was .505 msec faster, a P3 which was .953 msec faster, and a P4 which was 1.315 msec faster. A retest of the younger mice showed that much of this retrocochlear latency decrease occurred between 16 to 18 days postpartum. The latencies of the younger mice were also less likely to decrease as the stimulus intensity was increased from 30 to 70 dB, and this effect was most pronounced at higher neural levels. These age-related changes bear considerable relationship to the development of susceptibility of audiogenic seizures in the mouse. [ABSTRACT FROM AUTHOR]