Forward acoustic masking enhances the auditory brainstem response in a diotic, but not dichotic, paradigm in salicylate-induced tinnitus.

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.

Liu XP ，Chen L 《-》

Auditory brainstem response as a possible objective indicator for salicylate-induced tinnitus in rats.

The auditory response to an acoustic stimulus will usually be suppressed, or masked, by a preceding sound. Here, we show that forward acoustic masking at a high frequency can boost the auditory brainstem response (ABR) in rats injected with a high dose of sodium salicylate (NaSal), a tinnitus inducer. The forward narrow band noise caused a decrease in the amplitude of the ABR to a probe tone burst in normal rats, but caused an unexpected increase in the amplitude at 16 kHz in rats treated with NaSal (300 mg/kg). The observed effect could be manifested in normal rats presented with a background tone added to the masker and the probe, suggesting an underlying mechanism associated with tinnitus. We hypothesize that in NaSal-treated rats, tinnitus can "internally" mask the ABR in a similar way as an external background sound does and the "unmasking" effect of forward masking can result in a rebound of the otherwise suppressed ABR. Our study raises the possibility of using the ABR as an objective indicator for NaSal-induced tinnitus in animals. This article is part of a Special Issue entitled: Tinnitus Neuroscience.

Liu XP ，Chen L 《-》

Characterization of the perceived sound of trauma-induced tinnitus in gerbils.

Nowotny M ，Remus M ，Kössl M ，Gaese BH ... -  《-》

Central neural activity in rats with tinnitus evaluated with manganese-enhanced magnetic resonance imaging (MEMRI).

Brozoski TJ ，Ciobanu L ，Bauer CA 《-》

Evidence for differential modulation of primary and nonprimary auditory cortex by forward masking in tinnitus.

It has been proposed that tinnitus is generated by aberrant neural activity that develops among neurons in tonotopic of regions of primary auditory cortex (A1) affected by hearing loss, which is also the frequency region where tinnitus percepts localize (Eggermont and Roberts 2004; Roberts et al., 2010, 2013). These models suggest (1) that differences between tinnitus and control groups of similar age and audiometric function should depend on whether A1 is probed in tinnitus frequency region (TFR) or below it, and (2) that brain responses evoked from A1 should track changes in the tinnitus percept when residual inhibition (RI) is induced by forward masking. We tested these predictions by measuring (128-channel EEG) the sound-evoked 40-Hz auditory steady-state response (ASSR) known to localize tonotopically to neural sources in A1. For comparison the N1 transient response localizing to distributed neural sources in nonprimary cortex (A2) was also studied. When tested under baseline conditions where tinnitus subjects would have heard their tinnitus, ASSR responses were larger in a tinnitus group than in controls when evoked by 500 Hz probes while the reverse was true for tinnitus and control groups tested with 5 kHz probes, confirming frequency-dependent group differences in this measure. On subsequent trials where RI was induced by masking (narrow band noise centered at 5 kHz), ASSR amplitude increased in the tinnitus group probed at 5 kHz but not in the tinnitus group probed at 500 Hz. When collapsed into a single sample tinnitus subjects reporting comparatively greater RI depth and duration showed comparatively larger ASSR increases after masking regardless of probe frequency. Effects of masking on ASSR amplitude in the control groups were completely reversed from those in the tinnitus groups, with no change seen to 5 kHz probes but ASSR increases to 500 Hz probes even though the masking sound contained no energy at 500 Hz (an "off-frequency" masking effect). In contrast to these findings for the ASSR, N1 amplitude was larger in tinnitus than control groups at both probe frequencies under baseline conditions, decreased after masking in all conditions, and did not relate to RI. These results suggest that aberrant neural activity occurring in the TFR of A1 underlies tinnitus and its modulation during RI. They indicate further that while neural changes occur in A2 in tinnitus, these changes do not reflect the tinnitus percept. Models for tinnitus and forward masking are described that integrate these findings within a common framework.

Roberts LE ，Bosnyak DJ ，Bruce IC ，Gander PE ，Paul BT ... -  《-》