| Summary: | 碩士 === 國立成功大學 === 生理學研究所 === 95 === Tinnitus is the phantom sensation of sound in the absence of the corresponding external stimuli. Multiple over-doses of salicylate (SA) induced reversible tinnitus in humans and animals. Previous studies showed that SA-induced tinnitus was associated with an elevated hearing threshold (of about 15 dB) especially affecting high frequency regions (~10-16 kHz). On the other hand, SA was also reported in amplification of auditory evoked potentials. Whether SA produces same effects to different sound stimuli remained unclear. This knowledge is important for the understanding of pathophysiological mechanism of tinnitus. Brainstem auditory evoked potential (BAEP) reflect the electrophysiological activity of large numbers of neurons in the brainstem auditory pathway with acoustic stimulation. Here, we recorded BAEP from intra-cranial electrodes chronically implanted in freely moving rats before and after daily doses of SA (250 mg/kg/day, i.p.) over a period of 5 consecutive days. In order to assess the SA effect on the auditory brainstem including the inferior colliculus, which presumably is involved in the genesis of tinnitus, the active epi-dural recording electrode was placed about inferior colliculus (2mm from lamda on one side), and the reference electrode at the bregma. Average BAEP integrals in the post-stimulus 10 ms were taken as the response measure to clicks or tone bursts of systemically varied intensities. We found an elevation of threshold (about 10 dB) of BAEP to clicks after SA treatment and in addition signs of loudness recruitment. But, the BAEP to tone bursts of 16 kHz was sensitized (about 10 dB) after the same SA treatment and in addition signs of hyperacusis. Such enhanced sensitivity was not obvious in the low frequency region of 4 kHz. This is the first time that a differential effect of SA on BAEP from different sounds was observed in the same animal. We explain that such differential effect could be related, among other factors, to the different threshold of BAEP to clicks and to tones, and to the difference in the frequency composition of acoustic stimuli. The present results suggested that the mechanisms of tinnitus could involve turning on the automatic gain control of the descending auditory system at higher intensity levels after SA suppresses the cochlear inputs at low intensity levels.
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