Brain stimulation prevents neural downregulation and optimizes learning.

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 (N = 37, age range=18-35 years old). In the sham condition we observed a significant decline in task-evoked BOLD activity within the attention network after the training and no behavioral improvement, suggesting neural changes associated with cognitive training that are not evident in the behavioral data. Conversely, in the active parietal tRNS condition, stimulation prevented the early decline in task-evoked BOLD activity, resulting in a sustained BOLD response. This increase was observed particularly within key nodes of the dorsal-ventral attention network, including the bilateral anterior and posterior IPS and frontal eye field (FEF). These effects were statistically significant at both the network and ROI level (p < 0.05, FDR-corrected) and were specific to the visuospatial task. This increased BOLD activity correlated with improved performance. These results suggest that tRNS counteracts early neural adaptation during short training protocols by sustaining activity in task-relevant cortical regions to enable learning that would otherwise fail. Our study provides the first direct evidence that tRNS mitigates early neural downregulation and preserves functional response dynamics during learning in crucial task-related cortical areas. This demonstrates that, in the parietal cortex, training-induced plasticity is not accompanied by the 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.