Imaging rapid, use-dependent plasticity of structural and functional circuits in the adult somatosensory cortex

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As humans, we take for granted our abilities to form an accurate sensory perception of the outside world or learn new facets of a sensory-motor task that may be required on a day-to-day basis. For example, a new medical student will use their sense of touch to learn how to assess a patients' pulse, quality of breathing or perform a new surgery that requires dexterous maneuvering. In order for us to carry out these activities, the neuronal circuits within our brain must change by adjusting the strength of communication between existing connections or by forming new ones altogether. Although considerable progress has been made towards understanding how our brain changes, much of the work conducted thus far has been done in post-mortem tissue or using imaging techniques that cannot track the exceptionally fast responses of our brain in real-time. Consequently, very little is known about how tactile stimulation or learning can induce rapid structural and functional changes in the cerebral cortex of the intact, living brain. The primary aims of my research will be to use new imaging technologies that will allow me to visualize in the living animal, how the cerebral cortex actively processes tactile information or forms new circuits during sensory stimulation or whilst learning new tactile associations. Further, I will dissect the neurochemical and molecular mechanisms that trigger rapid changes in cerebral cortical circuitry. Performing these experiments will provide critical information regarding the neurobiological mechanisms that mediate rapid forms of sensory learning, habituation and sensitization. Furthermore, knowing how to tune or prime cortical circuits with a relatively innocuous form of tactile stimulation may facilitate the treatment of neuropathological conditions associated with aberrant cortical responsiveness (eg. phantom limb sensations, fibromyalgia, schizophrenia) or the recovery of functions after injury-induced disruptions to cortical circuits.