Several lines of evidence suggest that loss of central inhibition after deprivation of input from the ear (peripheral deafferentation) may be one cause of chronic tinnitus. Aging and acoustic trauma, the two most common causes of peripheral damage to the auditory system, each decrease input to central auditory structures. Loss of input to tonic inhibitory systems would release excitatory structures from inhibitory regulation. The increased activity resulting may be interpreted by more rostral structures in the auditory pathway as tinnitus. Down-regulation of gamma-amino butyric acid (GABA), a major inhibitory neurotransmitter of the central auditory pathway, is a potential mechanism for the loss of inhibition. Both animal studies and human clinical trials implicate loss of inhibition, and specifically loss of GABA function, in the development of acoustic trauma-induced tinnitus.