Human motor memory retention requires fronto-parietal circuit plasticity

Recent studies in human motor learning have documented the involvement of higher-order somatosensory regions, specifically the rostral parietal cortex (rPC), in learning and retention, with limited participation of primary motor cortex (M1). The absence of M1 involvement suggests the recruitment of alternative frontal regions to support learning. The dorsal premotor cortex (PMd) is a primary candidate given its role in movement planning and its anatomical connectivity with rPC. However, the functional contribution of PMd to retention and the nature of its interaction with the parietal cortex-whether they operate independently or as an integrated network-remains unknown. To address this, we used a visuomotor adaptation task in which participants adapted to altered visual feedback. Following the acquisition of the motor memory, continuous theta burst stimulation (cTBS) was applied to either M1, rPC, or PMd to assess their contribution to retention. In retention tests, 24 h later, disruption of PMd led to a significant impairment, confirming its role in visuomotor learning. Disruption of rPC similarly led to impairment, whereas disruption of M1 did not. Crucially, when rPC and PMd were disrupted simultaneously to test for independent effects, the resulting impairment was no greater than when either area was disrupted alone. These findings thus indicate that these areas are functionally interconnected in a motor learning circuit, such that disruption of either node results in a similar impairment. This supports a model of adaptation and learning in humans that relies on a distributed parietal-premotor network that is not dependent on M1.NEW & NOTEWORTHY This study provides direct evidence of motor learning-related plasticity in a cortical circuit involving sensory areas in rostral parietal cortex and premotor areas in frontal cortex. Using a visuomotor adaptation paradigm with cTBS, disruption of rostral parietal or dorsal premotor cortex impairs retention, whereas disruption of primary motor cortex does not. Disrupting both regions together causes no additional impairment, suggesting an interconnected learning circuit in humans and advancing understanding of cortical substrates of motor learning.