Cortical Processing and Organization in the Congenitally Deaf
Hearing loss is the third most common chronic disability, affecting one in ten Canadians. Moreover, while hearing loss is the most common birth defect in Canada, comparatively little is known about the brain reorganization that occurs as a result. Plasticity is the neural mechanism by which complex nervous systems adjust themselves to their environment. Adaptive, or compensatory plasticity is a part of this overall process resulting from the loss of a class (or modality) of sensory inputs that is accompanied by a corresponding expansion of the remaining systems. Not only does this process provide some substitute for the lost modality, but the additional circuitry also conveys enhanced abilities to the remaining systems. Examples of adaptive neuroplasticity include the apparent acoustic advantages of blind musicians and poets, and amplified visual performance in deaf individuals. However, there is debate on whether the primary sensory cortices are involved in this phenomenon and the specific higher-level brain circuitry and mechanisms that underlie this form of cross-modal effect are largely unidentified and unexamined.
These experiments are designed not only to elucidate the effects of early deafness on the brain, but also to develop and test a robust model of compensatory cross-modal plasticity through which basic principles governing the phenomenon are revealed and potential treatments may be evaluated and enhanced. The influence of neonatal deafness on the auditory cortices of mature animals will then be examined using a combination of mutually-reinforcing physiological, anatomical and behavioural techniques.
The first project is the identification of cross-modally reorganized auditory cortex following deafness. We are testing the hypothesis that there is a reverse hierarchical gradient in the level of cross-modal plasticity induced by neonatal deafening, where higher-order auditory cortices show more extensive cross-modal reorganization than primary/core areas. Extracellular electrophysiological recordings not only will examine specific cortices (areas AI, AAF, AII, PAF, and FAES) for cross-modal reorganization but, through the calculation of a quantitative cross-modal index, will also measure the degree to which the plasticity occurred. In this manner, the level of cross-modal reorganization in different regions will also be compared.
The second project examines the connectional basis for cross-modal reorganization of auditory cortex following deafness. We are testing the hypothesis that cross-modal cortical reorganization is primarily a consequence of modified thalamic inputs. In addition to examining possible changes in inputs to reorganized cortical areas, we are also examining cortical efferents emanating from these areas. Following neonatal deafening, we hypothesize that descending cortical projections from reorganized cortical areas to structures such as the superior colliculus will be relatively unchanged, while feedback projections to structures such as the inferior colliculus may be significantly altered.
The third project examines the behavioural significance of reorganized auditory cortex following deafness. We are testing the hypothesis that areas that have been physiologically reorganized in response to deafness are involved in behaviours that are similar to those of hearing animals, but are mediated by the replacement modality (vision). Behavioural tests combined with reversible cooling-deactivation of the selected cortical regions are being used to examine the relationship between cross-modally reorganized cortices and corresponding alterations in behaviour/perception.
Collectively, these results will provide new and comprehensive insight into the specific brain changes induced by early deafness to a level that is essentially unobtainable through other methods. In addition, these observations will form the basis for a robust and repeatable model of adaptive cross-modal plasticity that will be used to uncover the basic principles that characterize this phenomenon as well as better understand its relation to neuroplastic processes as a whole. Ultimately, future experiments could use such a model of cross-modal plasticity to empirically assess potential windows for therapeutic interventions.
These experiments are conducted in collaboration with Dr. Alex Meredith (Virginia Commonwealth University) and Dr. Andrej Kral (University of Hannover).