Abstract
Salicylate, the anti-inflammatory component of aspirin, induces transient tinnitus and hearing loss in clinical and animal experiments. However, the affected sites and mechanisms of generation remain unclear. Recently, down-regulation of inhibitory transmission mediated by γ-aminobutyric acid type A receptors was suggested to be crucial in generating tinnitus. However, the cell-specific pathways involved in this process were far from being understood. Here, we describe changes of inhibitory neurotransmitter, receptor, and glutamatergic axosomatic terminals in certain large GABAergic neurons (LGNs) in the inferior colliculus of rats treated with high doses of salicylate. Based on these results, we suggest that salicylate may affect inhibitory projection pathways from the inferior colliculus to the auditory cortex and lead to neural hyperactivity, perhaps by affecting the function of the LGNs.