Abstract
Aging-related changes have been identified at virtually every level of the central auditory system. One of the most common findings across these nuclei is a loss of synaptic inhibition with aging, which has been proposed to be at the heart of several aging-related changes in auditory cognition, including diminished speech perception in complex environments and the presence of tinnitus. Some authors have speculated that downregulation of synaptic inhibition is a consequence of peripheral deafferentation and therefore is a homeostatic mechanism to restore excitatory/inhibitory balance. As such, disinhibition would represent a form of maladaptive plasticity. However, clinical data suggest that deafferentation-related disinhibition tends to occur primarily in the aged brain. Therefore, aging-related disinhibition may, in part, be related to the high metabolic demands of inhibitory neurons relative to their excitatory counterparts. These findings suggest that both deafferentation-related maladaptive plastic changes and aging-related metabolic factors combine to produce changes in central auditory function. Here, we explore the arguments that downregulation of inhibition may be due to homeostatic responses to diminished afferent input vs. metabolic vulnerability of inhibitory neurons in the aged brain. Understanding the relative importance of these mechanisms will be critical for the development of treatments for the underlying causes of aging-related central disinhibition.
Highlights
Aging-related hearing loss is increasing in the population
Intelligibility of complex sounds is generally impaired beyond what can be explained with threshold or tuning shifts, suggesting that aging-related changes occur in the central auditory system that may not be solely explained by changes in the periphery
Aging is associated with alterations in a broad range of neurochemicals across auditory nuclei, in particular the inhibitory neurotransmitters gamma-amino-butyric acid (GABA)
Summary
Aging-related hearing loss is increasing in the population. There will be an approximately 50%. Decreases in synaptic inhibition in the aging central auditory system have been interpreted to be a consequence of a loss of peripheral input and to be an adaptive response to boost failing peripheral acoustic signals [11] In this context, diminished synaptic inhibition has been interpreted as being responsible for other pathological changes, such as increased spontaneous activity, diminished temporal fidelity, and perceptual changes, such as tinnitus and diminished ability to suppress distractors [12,13]. This view comports with a growing body of literature demonstrating that neural networks homeostatically adjust their overall magnitude of excitation and inhibition to maintain a balance between the two (reviewed in [14]). We review the evidence for each of these theories, and suggest experiments to test them
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