Salicylate toxicity model of tinnitus

Daniel Stolzberg,Richard J Salvi,Brian L Allman

doi:10.3389/fnsys.2012.00028

Abstract

Salicylate, the active component of the common drug aspirin, has mild analgesic, antipyretic, and anti-inflammatory effects at moderate doses. At higher doses, however, salicylate temporarily induces moderate hearing loss and the perception of a high-pitch ringing in humans and animals. This phantom perception of sound known as tinnitus is qualitatively similar to the persistent subjective tinnitus induced by high-level noise exposure, ototoxic drugs, or aging, which affects ∼14% of the general population. For over a quarter century, auditory scientists have used the salicylate toxicity model to investigate candidate biochemical and neurophysiological mechanisms underlying phantom sound perception. In this review, we summarize some of the intriguing biochemical and physiological effects associated with salicylate-induced tinnitus, some of which occur in the periphery and others in the central nervous system. The relevance and general utility of the salicylate toxicity model in understanding phantom sound perception in general are discussed.

Highlights

Subjective tinnitus is characterized by the perception of a sound in the absence of an acoustic source in the environment
The salicylate toxicity model differs from the noise trauma model of tinnitus in several respects; a few aspects shared by the two models may facilitate the identification of key brain regions and patterns of neural activity involved in tinnitus perception in general
PERIPHERAL OR CENTRAL? One critical aspect to understanding the origins of tinnitus is whether a persistent signal is generated in the ear or abnormal patterns of neural activity occur within the brain

Summary

Salicylate toxicity model of tinnitus

Salicylate temporarily induces moderate hearing loss and the perception of a high-pitch ringing in humans and animals. This phantom perception of sound known as tinnitus is qualitatively similar to the persistent subjective tinnitus induced by high-level noise exposure, ototoxic drugs, or aging, which affects ∼14% of the general population. For over a quarter century, auditory scientists have used the salicylate toxicity model to investigate candidate biochemical and neurophysiological mechanisms underlying phantom sound perception. We summarize some of the intriguing biochemical and physiological effects associated with salicylate-induced tinnitus, some of which occur in the periphery and others in the central nervous system.

INTRODUCTION

EFFECTS ON GABAergic NEUROTRANSMISSION

Findings

DISCUSSION