Animal models of salicylate-induced tinnitus have demonstrated that salicylate modulates neuronal activity in several brain structures leading to neuronal hyperactivity in auditory and non-auditory brain areas. In addition, these animal tinnitus models indicate that tinnitus can be a perceptual consequence of altered spontaneous neural activity along the auditory pathway. Peripheral and/or central effects of salicylate can account for neuronal activity changes in salicylate-induced tinnitus. Because of this ambiguity, an in vivo imaging study would be able to address the peripheral and/or central involvement of salicylate-induced tinnitus. Therefore, in the present study, we developed a novel manganese-enhanced magnetic resonance imaging (MEMRI) method to map the in vivo functional auditory tract in a salicylate-induced tinnitus animal model by administrating manganese through the round window. We found that acute salicylate-induced tinnitus resulted in higher manganese uptake in the cochlea and in the central auditory structures. Furthermore, serial MRI scans demonstrated that the manganese signal increased in an anterograde fashion from the cochlea to the cochlear nucleus. Therefore, our in vivo MEMRI data suggest that acute salicylate-induced tinnitus is associated with higher spontaneous neural activity both in peripheral and central auditory pathways.
Keywords: Auditory pathway; Gap prepulse inhibition of acoustic startle; Manganese-enhanced MRI; Salicylate; Tinnitus.
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