Altered stimulus-intensity encoding occurs in the primary somatosensory cortex of a central post-stroke pain rat model

Central post-stroke pain (CPSP) is a chronic form of pain that develops after ventral posterolateral thalamus (VPL) lesions and may involve maladaptive plasticity within central somatosensory pathways. Although abnormalities in the primary somatosensory cortex (S1) are observed in patients and animal models, the mechanism by which thalamic lesions alter cortical processing of sensory stimuli remains unclear. Here, we investigated stimulus intensity encoding and dendritic remodeling in S1 using a VPL–lesion CPSP rat model. Behavioral assessments were conducted, and mechanical allodynia was observed 3 weeks after lesion induction. Accordingly, the animals were examined during the early (1 week) and late (4–5 weeks) phases after VPL lesions. A distorted stimulus–response relationship was observed in S1 during the late phase, as indicated from voltage-sensitive dye imaging. The responses to low-intensity stimuli were enhanced, and response scaling at higher stimulus intensities was reduced. Increased cortical sensitivity to weak stimuli was associated with the severity of mechanical allodynia. Additionally, morphological analyses were conducted on layer II/III pyramidal neurons. Distinct patterns of dendritic remodeling were observed. Apical dendritic length and branching diminished during the early phase, while basal dendritic arborization increased during the late phase. These findings suggest that time-dependent structural and functional reorganization occurs in S1 following thalamic injury. This reorganization may contribute to abnormal sensory processing in patients with CPSP and offer new insights into the underlying pathophysiological mechanisms.