Synchrony in auditory 40-Hz gamma oscillations increases in older age and correlates with hearing abilities and cortical GABA levels

Abstract

Abstract Synchronized 40-Hz gamma oscillations in specific sensory and higher-order thalamocortical networks provide a neural mechanism for feature binding. Aging-related changes in gamma oscillations may cause deficits in auditory feature binding, contributing to impaired speech-in-noise perception. Gamma synchrony is controlled through inhibitory mechanisms mediated by the neurotransmitter γ-aminobutyric acid (GABA), which has been shown to decline in aging. This study investigated aging-related changes in gamma oscillations and how they relate to auditory function and cortical GABA levels. Magnetoencephalograms of 40-Hz auditory steady-state responses (ASSRs) were recorded in young and older adults by presenting amplitude-modulated tones in quiet and mixed with concurrent multi-talker babble noise. Responses in the quiet condition had longer latencies and more prominent amplitudes, indicating the 40-Hz ASSRs in noise were dominated by a sensory component and in quiet by a component involved in higher-order processing. The ASSR amplitudes increased in older adults under both stimulus conditions. However, larger ASSR amplitudes were associated with more severe hearing and speech-in-noise loss only in the noise condition. This suggests the aging-related increase in synchrony of sensory gamma oscillations has a detrimental effect on auditory processing. It may cause increased interference between competing sounds in the central auditory system, making it difficult for the aging auditory system to separate speech features from noise and bind them into a distinct perceptual object. Also in older adults, larger amplitudes of the 40-Hz ASSRs in the quiet condition were associated with higher left auditory cortex GABA concentrations measured with magnetic resonance spectroscopy, supporting GABA’s role in internally generated gamma synchrony in aging.