Electronic Thesis and Dissertation Repository

Degree

Doctor of Philosophy

Program

Anatomy and Cell Biology

Supervisor

Allman, Brian L.

Abstract

The consequences of hearing loss are not confined to how the central auditory system processes sound; crossmodal plasticity also occurs, which is characterized by an increased responsiveness of neurons in auditory areas to visual and/or tactile stimuli. In the primary auditory cortex, partial hearing loss causes a decrease in the number of auditory-responsive neurons, as well as an increase in multisensory neurons. However, it was relatively unknown how adult-onset hearing loss affected cortical areas that are already capable of integrating multisensory information, such as the lateral extrastriate visual cortex (V2L). Using a combination of in vivo electrophysiology, neuropharmacology and behavioural testing, this thesis investigated the nature and extent that crossmodal plasticity occurs within higher-order sensory cortices, and its perceptual consequences. At the level of single neurons, hearing loss increased the proportion of visually-responsive neurons, and decreased the number of neurons activated by both auditory and visual stimuli in V2L; findings inconsistent with the plasticity observed in the neighbouring dorsal auditory cortex (AuD), where the proportion of multisensory neurons nearly doubled. Subsequent analyses of the microcircuits within these higher-order cortices, revealed a layer-specific enhancement of auditory input (i.e., central gain enhancement) within the granular layer of AuD. In contrast, crossmodal plasticity was evident across multiple cortical layers within V2L, and also manifested in AuD. Despite the extensive plasticity in the higher-order sensory cortices, hearing loss lead to behavioural changes in audiovisual perception, characterized by a rapid recalibration of temporal sensitivity to the audiovisual stimuli. Next, a neurophysiological assessment revealed that adult-onset hearing loss did not cause a loss of temporally-precise audiovisual processing, but rather a shift in the cortical region displaying the capacity for temporal sensitivity. Lastly, using pharmacological manipulations, hearing loss was found to cause a layer-specific enhancement of visual-evoked input within the granular layer of the V2L cortex, indicative of thalamocortical plasticity. Overall, this work demonstrates that adult-onset hearing loss induces plasticity at the level of single neurons, local cortical microcircuits and sensory perception, all of which are associated with a complex assortment of crossmodal and intramodal changes across the layers of higher-order sensory cortices.

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