High doses of salicylate induce a temporary hearing deficit and a temporary subjective tinnitus in humans and animals. In animals, salicylate suppresses activity in the ascending auditory system but generates activity and plasticity in the auditory cortex and central amygdala. In addition to changes in the auditory system evoked by hearing impairment, enhanced stress may be crucial for the salicylate-induced alterations in the auditory cortex. The central amygdala responds to stress, and may influence cortical excitability and plasticity through cholinergic mechanisms. We investigated whether salicylate-induced plasticity in the auditory cortex is prevented by blocking cortical cholinergic receptors with the muscarinic antagonist scopolamine. Scopolamine suppresses salicylate-induced plasticity in the auditory cortex and, therefore, may be effective in suppressing the tinnitus sensation.