Effects of High-Intensity Sound Exposure on Neurotransmitter Chemistry in the Central Auditory System

Abstract

Exposure to intense sound often leads to tinnitus, the perception of a monotonous sound not actually present. Increased neural spontaneous activity in the central auditory system found in animal models of tinnitus should have a basis in their chemistry. Most chemical studies so far have focused on neurotransmitters, by which neurons communicate with each other, because alteration of this chemistry could easily lead to abnormal neural activity that might be perceived as tinnitus. Although increased spontaneous activity has been observed in the hamster dorsal cochlear nucleus (DCN) a month after intense tone exposure, we did not find increased glutamate concentrations in the 3 layers of the hamster dorsal DCN at that time. We did, however, find decreased glutamate concentrations 2 days after exposure that might correlate with slightly decreased spontaneous activity observed then. Others have provided evidence for decreased glutamate release in the chinchilla DCN 2 days after intense sound exposure. Other intense-sound-induced changes are increased choline acetyltransferase activity in some cochlear nucleus regions, increased acetylcholine receptor sensitivity in some DCN neurons, and some changes in the γ-aminobutyric acid (GABA) neurotransmitter system in the inferior colliculus. There is a need for more study of these and other neurotransmitter systems to determine their possible roles in tinnitus.