Tinnitus often develops following inner ear pathologies, like acoustic trauma. Therefore, an acoustic trauma model of tinnitus in gerbils was established using a modulated acoustic startle response. Cochlear trauma evoked by exposure to narrow-band noise at 10 kHz was assessed by auditory brainstem responses (ABR) and distortion product otoacoustic emissions (DPOAE). Threshold shift amounted to about 25 dB at frequencies > 10 kHz. Induction of a phantom-noise perception was documented by an acoustic startle response paradigm. A reduction of the gap-prepulse inhibition of acoustic startle (GPIAS) was taken as evidence for tinnitus at the behavioral level. Three to five weeks after trauma the ABR and DPOAE thresholds were back to normal. At that time, a reduction of GPIAS in the frequency range 16–20 kHz indicated a phantom noise perception. Seven weeks post trauma the tinnitus-affected frequency range became narrow and shifted to the center-trauma frequency at 10 kHz. Taken together, by investigating frequency-dependent effects in detail, this study in gerbils found trauma-evoked tinnitus developing in the frequency range bordering the low frequency slope of the induced noise trauma. This supports the theory of lateral inhibition as the physiological basis of tinnitus.
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