According to the microglial hypothesis of schizophrenia, the hyperactivation of microglia and the release of proinflammatory cytokines lead to neuronal loss, which is highly related to the onset of schizophrenia. Recent studies have demonstrated that fractalkine (CX3CL1) and its receptor CX3CR1 modulate the function of microglia. Thus, the present study aimed to determine whether microglial CX3CR1 plays a role in schizophrenia-related behaviors. A classical animal model of schizophrenia, social isolation (from postnatal days 21–56), was used to induce schizophrenia-related behaviors in C57BL/6J and CX3CR1^−/− mice, and the expression of the microglial CX3CR1 protein was examined in several brain areas of the C57BL/6J mice by Western blot analysis. The results revealed that social isolation caused deficits in the prepulse inhibition (PPI) in the C57BL/6J mice but not in the CX3CR1^−/− mice and increased locomotor activity in both the C57BL/6J mice and the CX3CR1^−/− mice. Moreover, the CX3CR1 protein level was increased in the medial prefrontal cortex, nucleus accumbens, and hippocampus of the isolated C57BL/6J mice. These findings suggested that the function of microglia regulated by CX3CR1 might participate in schizophrenia-related behaviors.

根据精神分裂症的小胶质细胞假说，小胶质细胞的过度活化和促炎性细胞因子的释放会导致神经元丢失，这与精神分裂症的发作高度相关。最近的研究表明，fractalkine（CX3CL1）及其受体CX3CR1调节小胶质细胞的功能。因此，本研究旨在确定小胶质细胞CX3CR1是否在精神分裂症相关行为中起作用。社会隔离（从出生后的第21-56天开始）是精神分裂症的经典动物模型，用于诱导C57BL / 6J和CX3CR1 ^-/-的精神分裂症相关行为小鼠，并通过蛋白质印迹分析在C57BL / 6J小鼠的多个脑区域检查了小胶质CX3CR1蛋白的表达。结果显示造成的C57BL / 6J小鼠的前脉冲抑制（PPI）的赤字，但社会不是孤立的CX3CR1 ^{- / -}小鼠和增加自主活动的C57BL / 6J小鼠和CX3CR1都^{- / -}小鼠。此外，CX3CR1蛋白水平增加了分离的C57BL / 6J小鼠的内侧前额叶皮层，伏隔核和海马中。这些发现表明，CX3CR1调控的小胶质细胞功能可能参与了精神分裂症相关行为。