No abstract

JSTOR is a not-for-profit service that helps scholars, researchers, and students discover, use, and build upon a wide range of content in a trusted digital archive. We use information technology and tools to increase productivity and facilitate new forms of scholarship. For more information about JSTOR, please contact support@jstor.org.. The National Institute of Environmental Health Sciences (NIEHS) andBrogan & Partners are collaborating with JSTOR to digitize, preserve and extend access to Environmental Health Perspectives.Evidence is presented to support the hypothesis that the cochleae of young animals are more susceptible to auditory trauma than the cochleae of the adult. A sensitive period of heightened susceptibility to acoustic trauma from noise exposure has been demonstrated in three mammalian species. The cochlear pathology associated with this trauma is severe damage to the outer hair cell system. Abnormal growth of auditory evoked responses recorded in central auditory nuclei accompanies the receptor damage during the sensitive period. There is evidence of a similar sensitive period of susceptibility to cochlear insult from ototoxic drugs. The time frame of the sensitive period may be different for drug or noise insult to the cochlea, but the principal pathology of outer hair cell loss remains the same in both cases. The implication of these sensitive periods to auditory trauma, for human development is considered.

No abstract

Evidence is presented to support the hypothesis that the cochleae of young animals are more susceptible to auditory trauma than the cochleae of the adult. A sensitive period of heightened susceptibility to acoustic trauma from noise exposure has been demonstrated in three mammalian species. The cochlear pathology associated with this trauma is severe damage to the outer hair cell system. Abnormal growth of auditory evoked responses recorded in central auditory nuclei accompanies the receptor damage during the sensitive period. There is evidence of a similar sensitive period of susceptibility to cochlear insult from ototoxic drugs. The time frame of the sensitive period may be different for drug or noise insult to the cochlea, but the principal pathology of outer hair cell loss remains the same in both cases. The implication of these sensitive periods to auditory trauma, for human development is considered.

Acoustic sensitization or priming for audiogenic seizures was studied in 304 “seizure‐resistant” mice of C57BL, BALB/c and their F1 hybirds. The effect of priming was found to be a function of strain, age of the first auditory exposure, and duration of exposure. In BALB/c mice priming at ages 21–28 days induced very high incidence of seizures; in this stran 2‐min exposure was more effective than both 60 sec or 30 sec. The same parameters of priming induced very low seizure incidence in C57BL mice. A behavior‐genetic analysis indicated that the genotype of each parental strain might contribute equally to the priming induced seizure risk of their F1 hybrids, but C57BL mice appeared to be dominant to the BALB/c for some components of audiogenic seizures.