Abstract

We recently reported that forward acoustic masking can enhance the auditory brainstem response (ABR) in rats treated with a high dose of sodium salicylate (NaSal), a tinnitus inducer, when tested in open acoustic field (Liu and Chen, 2012, Brain Research 1485, 88–94). In the present study, we first replicated this experiment in closed acoustic field under two conditions: (1) the forward masker and the probe were presented to both ears (diotic paradigm); (2) the forward masker was presented to one ear and the probe to the other ear (dichotic paradigm). We found that only when the stimuli were presented by using the diotic, rather than the dichotic, paradigm could forward acoustic masking enhance the ABR in the rat treated with NaSal (300 mg/kg). The enhancement was obvious for ABR waves II and IV, but not for wave I, indicating a central origin. The enhancement occurred at the high frequencies (16, 24, 32 kHz) at which the animals demonstrated a tinnitus-like behavior as revealed by using the gap prepulse inhibition of acoustic startle paradigm. We then administered vigabatrin, a GABA transaminase inhibitor, in the animals to suppress NaSal-induced tinnitus. The vigabatrin treatment successfully prevented forward acoustic masking from enhancing the ABR. These findings demonstrate that the observed enhancement of ABRs by forward acoustic masking originates in the central auditory pathway ipsilateral to the stimulated ear. We propose that the enhancement is closely associated with NaSal-induced tinnitus.

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