Reactive and adaptive remodeling of S1 cortical maps correlates with functional deficits and recovery following M1 microinfarct.

Reciprocal connections between the S1 and M1 cortices suggest a crucial role for somatosensory processing in cortical reorganization following M1 injury. However, the specific contribution of S1 to functional recovery after M1 lesions remains unclear. Here, we investigated remodeling of the S1 forepaw map alongside spontaneous sensorimotor recovery following a focal lesion to the caudal forelimb area (CFA) of M1. We also evaluated how a rehabilitation protocol influenced both cortical reorganization and behavioral outcomes. A microinfarct in the CFA induced marked alterations in the ipsilesional S1 forepaw cutaneous map and caused pronounced asymmetries in gross and fine forelimb sensorimotor tasks. These deficits were transient, with full recovery occurring within two months and significantly accelerated by rehabilitation. The cortical representation of the ventral skin gradually expanded beyond its pre-lesion size in association with behavioral recovery, while the representation of the dorsal skin remained unchanged. Initially, the lesion caused an expansion of both ventral and dorsal skin receptive fields (RFs), peaking at 14 days postlesion. Ventral RFs subsequently refined, becoming smaller than pre-lesion size, whereas dorsal RFs returned to baseline. Early rehabilitation accelerated RF shrinkage, particularly in ventral areas, mirroring late-stage spontaneous recovery. Neuronal sensitivity to light touch increased steadily post-lesion, with rehabilitation shortening this progression. The cutaneous RFs' sharpening and ventral cortical territory expansion closely paralleled recovery of fine sensorimotor skills. These findings highlight the pivotal role of S1 cortical plasticity in sensorimotor recovery following M1 injury and support early rehabilitation as a facilitator of adaptive cortical reorganization and functional recovery.