Abstract: Objective To observe the changes of chemokine receptor 1(CX3CR1) expression in neurons after cerebral ischemia, and to explore its function mechanism. Methods Wild-type C57/BL6 mice and CX3CR1 gene knockout mice were set up as control group (sham operation group) and permanent middle cerebral artery occlusion(pMACO) model, respectively. Cerebral ischemia range and infarction area were detected after 30min by MRI, and apoptosis was detected by immunofluorescence triple staining.Western blot was used to detect the expression of CX3CR1 protein.In vitro, primary neurons were cultured to establish an oxysaccharide dissection (OGD) cell ischemia model. Cell survival rate was detected by MTT colorimetry, expression of CX3CR1 on neurons was detected by immunofluorescence, and the changes of Ca²⁺ concentration in neurons was observed by laser confocal microscopy. Results Compared with the control group, the expression of CX3CR1 in affected side of pMACO significantly increased in wild-type mice (P＜0.05), and CX3CR1 was co-expressed with the apoptotic protein caspase-3 in neurons.Compared with wild-type ones, the ischemic injury area of CX3CR1 gene knockout mice was similar 30 min after pMACO, but the infarct area of CX3CR1 gene knockout mice 24 h after pMACO was smaller than that of the control group (P＜0.05).In vitro, the expression of CX3CR1 significantly increased after OGD of primary neurons (P＜0.05). Knockout of CX3CR1 on neurons can reduce the excitatory injury mediated by glutamate and significantly increase the cell survival rate. Meanwhile, the knockout of CX3CR1 reduces the speed and quantity of glutamate-mediated Ca²⁺ flowing into neurons. Conclusions Ischemia can induce the expression of CX3CR1 on neurons, and CX3CR1 on neurons mediates the apoptosis of neurons by regulating Ca²⁺ internal flow.

Key words: ischemia, CX3CR1, neurons, apoptosis, calcium ion