Abstract
Speech recognition and language learning can be affected by both peripheral and central auditory system impairment. However, whether sensorineural hearing loss would affect central auditory processing is not clear. Recent studies found that salicylate not only affects outer hair cell motility in the cochlea, but also blocks GABAergic neuron activities in central nervous systems. This provides a good animal model to evaluate the role of sensorineural hearing loss and central inhibition in auditory temporal processing. In this study, gap prepulse inhibition (gap-PPI) of the acoustic startle reflex was used to measure effects of salicylate on gap detection acuity. Salicylate administration (250 mg/kg) resulted in a significant reduction in gap-PPI amplitude and an increased gap detection threshold at 50 dB SPL, but not at 60 or 80 dB SPL. To identify the physiological effects of salicylate on central auditory system function, the inferior colliculus (IC) and auditory cortex (AC) responses were measured from conscious rats with chronically implanted electrodes. Salicylate induced a significant increase of the gap-detection threshold in AC-evoked potentials, but not in the IC-evoked potentials. The AC gap-detection threshold shift was diminished measured at an equal sensational level. These results suggest that salicylate-induced temporal processing deficits may be due to peripheral hearing loss, not central disinhibition.
Published Version
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