Modulation of learning-dependent plasticity in the attention network

Abstract

Non-invasive brain stimulation, such as transcranial random noise stimulation (tRNS), has been shown to enhance cortical excitability and facilitate perceptual learning. However, the neural mechanisms underlying these effects remain poorly understood. Here, we demonstrate that tRNS over the bilateral intraparietal sulcus (IPS) optimizes learning by preventing the decline in neural activity that occurs during short, high-load attentional training, thereby sustaining excitability and enhancing behavioral performance. Using a multi-session tRNS-fMRI paradigm, we investigated how tRNS modulates learning-related plasticity in the attention network during cognitive training. In the sham condition we observed a significant decline in task-evoked BOLD after the training and no behavioral improvement, suggesting crucial neural changes associated with cognitive training that are not evident in the behavioral data. Conversely, in the active tRNS condition, stimulation not only prevented the early decline in task-evoked BOLD activity observed in the sham condition, but it increased it. This change in BOLD activity correlated with improved performance. This suggests that tRNS counteracts early neural adaptation during short training protocols, sustaining activity in task-relevant cortical regions to enable learning that would otherwise fail. By providing the first direct evidence that tRNS mitigates early neural downregulation and preserves functional response dynamics during learning in crucial task-related cortical areas, our study demonstrates that in parietal cortex training-induced plasticity is not accompanied by efficiency-driven reductions in activation, like typically seen in sensory areas. Instead, we propose that sustaining neural excitability through tRNS prolongs plasticity and optimizes cognitive performance in higher order attentional areas. These findings highlight tRNS as a powerful tool for enhancing attentional learning and modulating neuroplasticity in both healthy and clinical populations.