Noise and the young mouse: genotype modifies the sensitive period for effects on cochlear physiology and audiogenic...

A sharply defined "critical period" has been described for the young C57BL/6 mouse, during which acoustic trauma will profoundly alter subsequent auditory behavior (audiogenic seizures, acoustic startle reflex). In several genotypes and species, a broader "sensitive period" exists, during which acoustic trauma is most damaging to cochlear functions in the young ear. In order to examine the correspondence of these two events, C57BL/6 and CBA inbred mice, at eight ages ranging from 12 to 54 days, were exposed to 2 min of a 124-dB (SPL) octave band noise (8-16 kHz). A noninvasive electrocochleographic technique was used to assess cochlear microphonic (CM) and action potential (AP) thresholds in exposed mice and their nonexposed littermate controls. This allowed cochlear functional measures and behavioral tests (susceptibility to audiogenic seizures) to be made in the same animals. Noise has no observable effect on the 12-day-old CBA mouse, produced a maximal threshold elevation (47 dB for AP, 28 dB for CM) at 30-36 days, with the effect declining to nearly half of this value in 54-day-old subjects. Susceptibility to audiogenic seizures in the exposed CBA mice was greatest at the peak of this sensitive period for cochlear damage (r = .95). C57BL/6 mice also appeared unaffected when noise exposure occurred at 12 days of age; they had maximal AP (23 dB) and CM (17 dB) threshold elevations at 36 days, and 54-day-old mice had an 18-dB elevation of the AP and their CM was no longer affected. Susceptibility to audiogenic seizures was greatest in C57BL/6 mice exposed to noise at 18 days, and it did not correspond with the sensitive period for cochlear damage (r = .21). Therefore, both genotypes have a sensitive period for the effects of noise trauma on the CM and AP, the CBA has a sensitive period for acoustic priming for audiogenic seizures, and the C57BL/6 has a critical period for acoustic priming. Genetic differences in age-related losses of central nervous system auditory functions are postulated as being responsible for these behavioral differences. These data are compared with known auditory functions of the SJL and BALB/c mouse strains in order to explain genetically determined differences of the sensitive (or critical) period of acoustic priming, and for the length of time the mice subsequently remain susceptible to audiogenic seizures.