Abstract

To test the “tinnitus gap-filling” hypothesis in an animal psychoacoustic paradigm, rats were tested using a go/no-go operant gap detection task in which silent intervals of various durations were embedded within a continuous noise. Gap detection thresholds were measured before and after treatment with a dose of sodium salicylate (200 mg/kg) that reliably induces tinnitus in rats. Noise-burst detection thresholds were also measured to document the amount of hearing loss and aid in interpreting the gap detection results. As in the previous human psychophysical experiments, salicylate had little or no effect on gap thresholds measured in broadband noise presented at high-stimulus levels (30–60 dB SPL); gap detection thresholds were always 10 ms or less. Salicylate also did not affect gap thresholds presented in narrowband noise at 60 dB SPL. Therefore, rats treated with a dose of salicylate that reliably induces tinnitus have no difficulty detecting silent gaps as long as the noise in which they are embedded is clearly audible.

Highlights

  • The ototoxic effects of high doses of salicylate, the active ingredient in aspirin, are well-established [1,2,3,4]

  • For baseline and saline conditions, mean BBN gap detection thresholds increased slightly from ~2 to 3 ms as the sound level decreased from 60 to 30 dB SPL, but at 20 dB SPL, gap thresholds increased to 4–6 ms

  • A two-way repeated measures analysis of variance (ANOVA) of the baseline and saline gap threshold obtained at 20–60 dB SPL showed a significant effect of intensity (F = 15.77, 3 df; p < 0.001) and a significant interaction between intensity and baseline and saline conditions (F = 11.79, Procedure The spectra of the noise-burst stimuli used in the noise detection experiments were the same as in the gap detection study, namely, BBN and the three narrowband noise (NBN) (10–20, 16–20, and 15.3–16.7 kHz)

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Summary

Introduction

The ototoxic effects of high doses of salicylate, the active ingredient in aspirin, are well-established [1,2,3,4]. A recent review by Sheppard et al [5] details the peripheral and central effects of salicylate along with the known perceptual deficits seen in humans following large doses of aspirin [5]. With moderate doses of aspirin, McFadden et al [13] found increased gap detection thresholds (impaired temporal resolution) at low sound-pressure levels and flatter than normal temporal integration functions (impaired temporal integration). These aspirin-induced changes in temporal resolution and temporal integration are similar to the temporal processing deficits seen in listeners with sensorineural hearing loss [14, 15]. Aspirininduced hearing loss has been proposed as a model of temporary sensorineural hearing loss in humans [13]

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