Homeostatic plasticity drives tinnitus perception in an animal model

TLDR

Hearing loss frequently causes tinnitus and cortical map changes, suggesting a link between phantom perception and cortical reorganization. High‑frequency hearing loss creates two cortical regions: a sensory‑deprived area with reduced inhibition and a normal‑hearing area with increased inhibition, excitation, and map reorganization. Tinnitus in hearing‑lesioned animals matched the loss frequency, was reversible by drugs enhancing inhibition but not by reducing excitation, indicating that homeostatic down‑regulation of inhibition contributes to tinnitus and that map reorganization could alleviate it.

Abstract

Hearing loss often results in tinnitus and auditory cortical map changes, leading to the prevailing view that the phantom perception is associated with cortical reorganization. However, we show here that tinnitus is mediated by a cortical area lacking map reorganization. High-frequency hearing loss results in two distinct cortical regions: a sensory-deprived region characterized by a decrease in inhibitory synaptic transmission and a normal hearing region showing increases in inhibitory and excitatory transmission and map reorganization. Hearing-lesioned animals displayed tinnitus with a pitch in the hearing loss range. Furthermore, drugs that enhance inhibition, but not those that reduce excitation, reversibly eliminated the tinnitus behavior. These results suggest that sensory deprivation-induced homeostatic down-regulation of inhibitory synapses may contribute to tinnitus perception. Enhancing sensory input through map reorganization may plausibly alleviate phantom sensation.