Henry K R
Behav Neurosci. 1984 Dec;98(6):1073-82. doi: 10.1037//0735-7044.98.6.1073.
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.
已描述了幼龄C57BL/6小鼠存在一个界限分明的“关键期”，在此期间，声损伤会深刻改变随后的听觉行为（听源性惊厥、听觉惊吓反射）。在几种基因型和物种中，存在一个更宽泛的“敏感期”，在此期间，声损伤对幼龄耳朵的耳蜗功能损害最大。为了研究这两个时期的对应关系，将12至54日龄的8个年龄段的C57BL/6和CBA近交系小鼠暴露于2分钟的124分贝（声压级）倍频程带噪声（8 - 16千赫）中。使用一种非侵入性的电耳蜗图技术评估暴露小鼠及其未暴露的同窝对照小鼠的耳蜗微音电位（CM）和动作电位（AP）阈值。这使得能够在同一动物身上进行耳蜗功能测量和行为测试（对听源性惊厥的易感性）。噪声对12日龄的CBA小鼠没有可观察到的影响，在30 - 36日龄时产生最大阈值升高（AP为47分贝，CM为28分贝），在54日龄的小鼠中，这种影响降至该值的近一半。暴露的CBA小鼠对听源性惊厥的易感性在耳蜗损伤敏感期的峰值时最高（r = 0.95）。当在12日龄时暴露于噪声时，C57BL/6小鼠似乎也未受影响；它们在36日龄时AP（23分贝）和CM（17分贝）阈值升高最大，54日龄的小鼠AP升高18分贝，且其CM不再受影响。在18日龄暴露于噪声的C57BL/6小鼠中，对听源性惊厥的易感性最高，且与耳蜗损伤的敏感期不对应（r = 0.21）。因此，两种基因型对噪声损伤对CM和AP的影响都有一个敏感期，CBA对听源性惊厥的声启动有一个敏感期，而C57BL/6对声启动有一个关键期。据推测，中枢神经系统听觉功能与年龄相关的损失方面的基因差异是造成这些行为差异的原因。将这些数据与已知的SJL和BALB/c小鼠品系的听觉功能进行比较，以解释声启动的敏感（或关键）期的基因决定差异，以及小鼠随后对听源性惊厥保持易感性的时间长度。
