Current view of neurotransmitter changes underlying tinnitus.

Abstract

Tinnitus is the perception of a monotonous sound not present in the environment. Nearly 20% of the U.S. population suffers from tinnitus, and tinnitus has been reported to be the most prevalent service-connected disability of all U.S. veterans (Henry et al., 2005; Eggermont, 2012; Veterans Benefits Administration, 2014). Many types of peripheral injury have been understood to induce tinnitus, including damage to the cochlea by intense sound or ototoxic medications and destruction of the auditory nerve by cochlear ablation or nerve transection (Lee and Godfrey, 2014). The pathophysiological mechanisms by which tinnitus develops are only poorly understood. In order to further clarify the pathogenesis, a need has been expressed for a better understanding of the rebalancing of excitatory and inhibitory signaling mechanisms that occur after peripheral injury (Gold and Bajo, 2014). One of the current, prominent hypotheses of tinnitus development is that, after being triggered by peripheral injury, tinnitus may result from a maladaptation of the central auditory system to this peripheral dysfunction (Auerbach et al., 2014), and that one of the mechanisms by which this occurs is a decrease in inhibitory neurotransmission. The major structures that play a role in transmitting neural activity through the ascending central auditory system include the cochlear nucleus and superior olivary complex of the pons-medulla region, the inferior colliculus of the midbrain, the medial geniculate nucleus of the thalamus, and the auditory cortex.