ABERRANT PLASTICITY OF THE MOTOR CORTEX ACTIVITY AND CONNECTIVITY IN A RAT MODEL OF CENTRAL POST-STROKE PAIN

Central post-stroke pain (CPSP) is a chronic neuropathic pain condition caused by stroke lesions in sensory relay nuclei, particularly the thalamus. However, time-dependent changes in neural activity in animals with CPSP induced by thalamic stroke remain unclear. Therefore, using flavoprotein autofluorescence imaging (FAI), we investigated time-dependent changes in neural activity in a CPSP rat model, and further assessed the structural brain alterations underlying these activity changes using diffusion tensor imaging (DTI) and neuronal tracer methods. In the model rats used in this study, behavioral changes indicative of CPSP development were observed beginning 2 weeks post-stroke. FAI results showed that neural activity in the secondary motor cortex (M2) was increased at 2 and 4 weeks post-stroke, compared to the control group. Additionally, pharmacological experiments suggested that the increased activity in M2 originates from the primary somatosensory cortex at 2 weeks post-stroke, but not at 4 weeks post-stroke. DTI revealed an increased number of tracts connecting the M2, primary motor cortex, and the ventral posteromedial thalamic nucleus at 4 weeks post-stroke compared to the control group. Similar results were also obtained from neuronal tracer analyses of the M2–M1 circuit. These findings suggest that increased M2 activity in CPSP is supported by distinct functional and structural neural mechanisms at 2 and 4 weeks post-stroke. Future studies should examine the causal relationship between pain and the neural circuits showing post-stroke plasticity identified in this study, using genetic techniques.