The current study used a rat model to investigate the underlying mechanisms of blast-induced tinnitus, hearing loss, and associated traumatic brain injury (TBI). Seven rats were used to evaluate behavioral evidence of tinnitus and hearing loss, and TBI using magnetic resonance imaging following a single 10-msec blast at 14 psi or 194 dB sound pressure level (SPL). The results demonstrated that the blast exposure induced early onset of tinnitus and central hearing impairment at a broad frequency range. The induced tinnitus and central hearing impairment tended to shift towards high frequencies over time. Hearing threshold measured with auditory brainstem responses also showed an immediate elevation followed by recovery on day 14, coinciding with behaviorally-measured results. Diffusion tensor magnetic resonance imaging results demonstrated significant damage and compensatory plastic changes to certain auditory brain regions, with the majority of changes occurring in the inferior colliculus and medial geniculate body. No significant microstructural changes found in the corpus callosum indicates that the currently adopted blast exposure mainly exerts effects through the auditory pathways rather than through direct impact onto the brain parenchyma. The results showed that this animal model is appropriate for investigation of the mechanisms underlying blast-induced tinnitus, hearing loss, and related TBI. Continued investigation along these lines will help identify pathology with injury/recovery patterns, aiding development of effective treatment strategies.

Recent clinical studies have demonstrated that auditory cortex electrical stimulation (ACES) has yielded promising results in the suppression of patients' tinnitus. However, the large variability in the efficacy of ACES-induced suppression across individuals has hindered its development into a reliable therapy. Due to ethical reasons, many issues cannot be comprehensively addressed in patients. In order to search for effective stimulation targets and identify optimal stimulation strategies, we have developed the first rat model to test for the suppression of behavioral evidence of tone-induced tinnitus through ACES. Our behavioral results demonstrated that electrical stimulation of all channels (frequency bands) in the auditory cortex significantly suppressed behavioral evidence of tinnitus and enhanced hearing detection at the central level. Such suppression of tinnitus and enhancement of hearing detection were respectively demonstrated by a reversal of tone exposure compromised gap detection at 10-12, 14-16, and 26-28 kHz and compromised prepulse inhibition at 10-12 and 26-28 kHz. On the contrary, ACES did not induce behavioral changes in animals that did not manifest any behavioral evidence of tinnitus and compromised hearing detection following the same tone exposure. The results point out that tinnitus may be more related to compromised central auditory processing than hearing loss at the peripheral level. The ACESinduced suppression of behavioral evidence of tinnitus may involve restoration of abnormal central auditory processing.

Exposure to high-pressure blast shock waves is known to cause tinnitus. Although the underlying mechanisms may involve damage to structures in the ear and/or direct brain impact, which triggers a cascade of neuroplastic changes in both auditory and nonauditory centers, it remains unclear how the induced neuroplasticity manifests neurophysiologically. This study investigates the influence of blast exposure on spontaneous firing rates (SFRs) in the dorsal cochlear nucleus (DCN) and its time course in rats with blast-induced tinnitus. Each rat was exposed to a single blast at 22 psi. Behavioral evidence of tinnitus was measured by using a gap-detection acoustic startle-reflex paradigm. SFRs were measured 1 day, 1 month, and 3 months after blast exposure. The results showed that nine rats with blast-induced tinnitus and hearing loss developed hyperactivity immediately and that the induced hyperactivity persisted in six rats with tinnitus at 1 month after blast exposure. At 3 months after blast exposure, however, the induced hyperactivity of four rats with tinnitus transitioned to hypoactivity. In addition, the 20-30-kHz, and >30-kHz regions in the DCN of rats with and without blast-induced tinnitus were more affected than other frequency regions at different recovery time points after blast exposure. These results demonstrate that the neural mechanisms underlying blast-induced tinnitus are substantially different from those underlying noise-induced tinnitus.

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