Abstract
Tinnitus, the perception of a monotonous sound not actually present in the environment, affects nearly 20% of the population of the United States. Although there has been great progress in tinnitus research over the past 25 years, the neurochemical basis of tinnitus is still poorly understood. We review current research about the effects of various types of cochlear damage on the neurotransmitter chemistry in the central auditory system and document evidence that different changes in this chemistry can underlie similar behaviorally measured tinnitus symptoms. Most available data have been obtained from rodents following cochlear damage produced by cochlear ablation, intense sound, or ototoxic drugs. Effects on neurotransmitter systems have been measured as changes in neurotransmitter level, synthesis, release, uptake, and receptors. In this review, magnitudes of changes are presented for neurotransmitter-related amino acids, acetylcholine, and serotonin. A variety of effects have been found in these studies that may be related to animal model, survival time, type and/or magnitude of cochlear damage, or methodology. The overall impression from the evidence presented is that any imbalance of neurotransmitter-related chemistry could disrupt auditory processing in such a way as to produce tinnitus.
Highlights
AN EMERGING ISSUE FOR SOCIETY Tinnitus, the perception of a monotonous sound, most commonly ringing (1), not present in the environment, can result from many different types of cochlear damage, including especially those resulting from acoustic trauma and ototoxic drugs (1, 2)
We have found different effects on central auditory system neurotransmitter systems of different types of cochlear damage, including partial damage from acoustic trauma (7–10) and carboplatin treatment (11, 12), both of which have been associated with tinnitus (2, 13), and complete destruction via cochlear ablation (14–17)
CLINICAL APPLICATIONS The compiled results from available studies suggest that different types of cochlear damage may lead to different neurotransmitterrelated chemical changes in the central auditory system, even though they all could result in tinnitus
Summary
AN EMERGING ISSUE FOR SOCIETY Tinnitus, the perception of a monotonous sound, most commonly ringing (1), not present in the environment, can result from many different types of cochlear damage, including especially those resulting from acoustic trauma and ototoxic drugs (1, 2). We have found different effects on central auditory system neurotransmitter systems of different types of cochlear damage, including partial damage from acoustic trauma (7–10) and carboplatin treatment (11, 12), both of which have been associated with tinnitus (2, 13), and complete destruction via cochlear ablation (14–17). The purpose of this review is to compare the effects of various types of cochlear damage on the neurotransmitter chemistry in the central auditory system, thereby to document evidence that different changes in this chemistry can underlie similar behaviorally measured tinnitus symptoms. Glutamine is closely related metabolically to glutamate as an important precursor (40, 41), predominantly located in glial cells (42) Both glycine and γ-aminobutyric acid (GABA) are well established as inhibitory neurotransmitters of the central auditory system, especially in the cochlear nucleus (CN), superior olive, and inferior colliculus (IC) (35, 43–55). No volume changes in CN regions were found after carboplatin administration (11)
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