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 Hamburg).