Microglia-mediated abnormal synaptic pruning via neuroinflammation and complement C1q activation constitutes a key pathological mechanism of PTSD
This study aims to explore the key pathological role of abnormal synaptic pruning mediated by microglia through neuroinflammation and complement C1q activation in PTSD, and to focus on verifying the regulatory mechanism of microglia-mediated neuroinflammation and complement C1q activation on the pathogenesis of PTSD. The specific procedures include: constructing a PTSD model mouse, randomly dividing the mice into a minocycline group (administered orally at 25 mg/kg/day for 7 days), a meloxicam group (intraperitoneally injected at 2.5 mg/kg/time, three times a day for 7 days), and a control group (no drug intervention after stress modeling). Subsequently, fear memory was assessed through a conditioned fear test, anxiety-like behaviors were detected through an elevated plus-maze test (recording the time spent in the open arms and the number of entries), and an open field test. After sacrificing the mice, their hippocampus tissues were collected, and C1q protein levels were detected by ELISA, and the expression of synaptic-related proteins (PSD-95, Synaptophysin) was analyzed by Western blot. Combined with transcriptome sequencing, the regulatory mechanism of microglia through neuroinflammation and complement C1q activation on synaptic pruning and PTSD pathology was systematically analyzed.