Imaging Brain Function in People with Tinnitus

were fundamentally different from those evoked by a real sound, we proposed that tinnitus originates in the brain. To identify potential drugs to treat tinnitus, we developed rat behavioral models of tinnitus. Like humans, rats exposed to high intensity noise developed tinnitus; in some cases, the tinnitus was transient while in others it was persistent. Humans develop tinnitus after taking high doses of aspirin (salicylate). Rats treated with high doses of salicylate reliably developed behavioral evidence of tinnitus. Memantine and scopolamine have been proposed as treatments for tinnitus, but neither drug suppressed salicylate-induced tinnitus. However, tinnitus was completely suppressed by a potassium channel modulator. We evaluated the neural correlates of salicylate-induced tinnitus along the auditory pathway. High doses of salicylate suppressed otoacoustic emissions and the compound action potential from the auditory nerve. Despite the fact that salicylate suppressed the neural output from the cochlea, it caused a large increase in the sound-evoked activity in the auditory cortex. That is, the auditory cortex became hyperactive after salicylate-induced hearing loss, a possible neural correlate of hyperacusis or sound intolerance; however, salicylate caused a significant decrease in spontaneous activity. These results suggest that the central auditory system becomes hyperactive following cochlear damage. This hyperactivity may be due to a loss of centrally mediated inhibition.