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Over the past two decades, considerable progress has been made in understanding the mechanisms underlying aminoglycoside ototoxicity. Aminoglycoside damage progresses from cochlear base to apex and from outer to inner hair cells. Aminoglycoside antibiotics enter hair cells at the apical pole and are taken up into lysosomes and mitochondria. Aminoglycosides generate damaging reactive oxygen species that can initiate a program of cell death. In cases of acute ototoxicity involving high doses of aminoglycosides, hair cells appear to die by apoptosis and their cuticular plates can be ejected from the epithelium. However, after long-term systemic administration, hair cell death occurs by either necrosis or apoptosis. Aminoglycoside ototoxicity is exacerbated by loop diuretics that accelerate drug entry into cochlear fluids resulting in rapid cell death. Knowledge of the signaling pathways involved in aminoglycoside ototoxicity has led to new strategies for preventing ototoxicity, involving antioxidants, protease inhibitors and neurotrophic factors. Such fundamental knowledge may one day lead to clinical procedures that block the ototoxic side effects of this important class of antibiotics. [ABSTRACT FROM AUTHOR]

A positive reinforcement conditioning procedure was used to train chinchillas to respond to intensity differences between successively occurring tone bursts. Intensity difference limens were measured at 0.5, 1, 4, and 8 kHz at five intensities ranging from 10- to 55-dB sensation level. The intensity difference limen decreased from approximately 8 dB near threshold to approximately 3.5 dB at the highest level. The intensity difference limens for the chinchilla were considerably larger than those for humans as well as several other mammals; however, the results were similar to those obtained for the parakeet. The present results from intensity discrimination appeared to be related to previous data for the discrimination of amplitude modulated noise. [ABSTRACT FROM AUTHOR]

The equal energy hypothesis (EEH) was evaluated over a limited range of conditions by exposing four groups of chinchillas to impact noise (200-ms B duration) presented at a fixed rate of four impacts per second. The intensity of the impacts (107-125 dB peak SPL) and the duration (120-1.87 h) of the four exposure conditions were counterbalanced so that the four groups received the same total energy. The traumatic power of the exposures was assessed by measuring the threshold shift of the auditory evoked response and the amount of hair cell loss. Exposures between 107 and 119 dB were consistent with the EEH in that they produced roughly the same amount of permanent threshold shift (less than 20 dB) and hair cell loss (less than 20%). However, the 125-dB exposure produced substantially more threshold shift and hair cell loss than the three lower intensities. Thus, the EEH may be applicable only at lower impact intensities; above a ''critical intensity'' the amount of damage increases significantly. [ABSTRACT FROM AUTHOR]

Auditory temporal resolution is known to deteriorate with sensorineural hearing loss; however, there is considerable intersubject variability in human studies. The purpose of the present study was to obtain measures of temporal resolution in the chinchilla as the degree of noise-induced hearing loss was systematically varied. Gap-detection thresholds, a measure of temporal resolution, were evaluated at four levels of noise-induced asymptotic threshold shift (ATS). Gap thresholds were normal when the pure-tone thresholds were elevated approximately 15 dB. With a hearing loss of approximately 30 dB, the gap thresholds were longer than normal if compared at the same sound pressure level, but within normal limits if compared at the same sensation level. When the hearing loss exceeded 40 dB, gap thresholds were longer than normal both in terms of sound pressure level and sensation level. These results show that there is an orderly breakdown in temporal resolution as the degree of noise-induced ATS increases. The results are related to neural data and models of temporal resolution. [ABSTRACT FROM AUTHOR]