内侧前额叶皮层介导6-OHDA小鼠痛敏反应的机制研究

Objective: This study aimed to investigate the regulatory role and mechanism of the medial prefrontal cortex (mPFC) in pain hypersensitivity in 6-OHDA-induced Parkinson\'s disease (PD) mice. Methods: Male C57BL/6J mice were used in the experiment. PD models were established by stereotactic injection of 6-OHDA into the right medial forebrain bundle (MFB). The von Frey and tail flick tests were used to detect changes in pain threshold, and the tail suspension, open field, and elevated plus maze tests were used to evaluate negative emotional changes. The number of c-Fos positive neurons in the mPFC was detected by c-Fos immunofluorescence staining, and their neuronal types were identified. The role of glutamatergic neurons in the mPFC in pain-related behaviors was detected by chemogenetic combined with behavioral methods. Results: Compared with the Sham group, the pain threshold of 6-OHDA group mice decreased significantly, the tail suspension immobility time increased, and the activity time in the center area of the open field and the open arm of the elevated plus maze decreased. The number of c-Fos positive neurons in the mPFC of 6-OHDA mice increased, and 70% of them were co-localized with glutamatergic neurons. After activating glutamatergic neurons in the mPFC, the pain threshold of 6-OHDA mice decreased. Inhibition had the opposite effect. Conclusion: The mPFC regulates pain hypersensitivity in 6-OHDA-induced PD mice, which may be related to the abnormal activation of glutamatergic neurons.