Studies of Cortical Plasticity in the Normal and the Diseased Brain

Despite the large amount of work that has been conducted since Donald’s Hebb work and described in his famous dissertation “The Organization of Behavior” (Hebb, 1949), understanding the experience-dependent mechanisms of plasticity within the primary visual cortex (V1) remains a major priority. Although plasticity effects are strongest during the critical period (early development), studies on cortical plasticity from the last two decades have clearly demonstrated that the human brain is plastic and amenable to changes throughout life. Perceptual Learning (PL) is one of the most commonly used procedure to promote visual improvement in neurotypicals and recovery of functions in a variety of disorders. However, a common feature to most of the training protocols is that they require long time and a high number of sessions to show effective improvement. Recently, non-invasive brain stimulation (NIBS) techniques, specifically transcranial random noise stimulation (tRNS) and anodal tDCS, have been used to modulate activity within the visual cortex to enhance perceptual learning. However, the mechanisms of action and the long-term effects on learning are still unknown. The questions this thesis work will address are the following: (1) can neuromodulatory techniques be used to boost visual perceptual learning in neurotypicals, which technique is the most effective and what are the long term effects on learning? (2) what are the potential underlying physiological mechanisms modulating cortical excitability of the visual cortex? and (3) contingent upon results from (1), can NIBS be used over early, peri-lesional visual areas during visual training to induce recovery of visuo-perceptual abilities in chronic partial cortical blindness (CB)? I used tRNS coupled with visuo-perceptual training protocols to promote fast and sustained perceptual learning in neurotypicals. I then provide evidence that tRNS can increase cortical excitability of the visual cortex, measured by priming early visual areas with tRNS, before measuring phosphene threshold with single pulse TMS. Lastly, I provide preliminary