Abstract:

Objective Explore the pathological mechanism of stroke hyperalgesia by using a rat model of thalamic BDNF signaling. Methods Wistar male rats（8 weeks old）were used in the study. The model of focal cerebral ischemia and reperfusion in rats were established by middle cerebral artery occlusion （MCAO）. The change of thermal pain threshold were assessed by hot plate tests. The rats were divided into two groups randomly： SHAM and central post ⁃stroke pain（CPSP）. Rats with hyperalgesia 3 days after surgery were screened for the post⁃stroke central pain group. TTC staining，HE staining，Nissl staining and Neun immunohistochemical staining were used to assess thalamus damage. Immunofluorescence was used to detect the number of activated microglia and BDNF. The expression of BDNF，TrkB and GABAAR proteins was determined by Western blot. Results When compared to the SHAM group，the CPSP rats had a significantly higher neurological deficit score，a lower heat pain threshold，thalamic VPL pathology injury，a lower number of nissl body and Neun positive expression， higher microglia and BDNF expression，higher thalamic BDNF and Trkb protein expression，and lower GABAAR protein expression. Conclusions Ischemia/reperfusion cerebral injury can result in hyperalgesia，with a 30% dis⁃ ease incidence. The concomitant BDNF ⁃Trkb of thalamic microglia activation plays a major role in mediating the pathological progression of hyperalgesia after stroke.

Key words:

central post ? stroke pain, thalamus, hyperalgesia, microglia, brain ? derived neuro? trophic factor, tyrosine kinase receptor B