Key result
Noise priming at day 18 induces audiogenic seizures and causes a ~30-dB cochlear sensitivity loss.
Why the study?
The physiological effects of priming with noise on cochlear microphonic sensitivity and audiogenic seizures in mice at various ages were not fully understood.
Priming C57BL/6J mice with noise at 18 days of age induces a 30-dB loss in cochlear microphonic sensitivity and susceptibility to audiogenic seizures, supporting the disuse-supersensitivity hypothesis.
Suggests narrow developmental window for audiogenic seizure priming in mice; hypothesis-generating for critical periods in mammalian auditory research.
Groups of mice were briefly exposed to a one-octave band of noise at 14, 18, 28, 38, or 58 days of age. Five days later the groups were divided, and some mice were behaviorally tested for audiogenic seizures by reexposing them to the same sound. The round window cochlear microphonic potential was measured in the remaining animals and compared with that observed in unprimed control subjects. Seizure behavior occurred in all animals primed on Day 18 but rarely for subjects in the other age groups. Cochlear microphonic threshold curves in mice primed on Day 18 showed a 30-dB loss in sensitivity, while all other primed groups showed little change. These data were discussed in terms of the "disuse-supersensitivity" hypothesis previously proposed to account for the physiological effects of priming in mice.
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Saunders et al. (1976) studied Audiogenic seizures. Exposure to a one-octave band of noise (priming) vs. Unprimed control subjects was evaluated on Seizure behavior and cochlear microphonic threshold curves. Priming C57BL/6J mice with noise at 18 days of age resulted in audiogenic seizure behavior and a 30-dB loss in cochlear microphonic sensitivity, whereas other age groups showed little change.
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