Xiao Feng, Xu Jun-Mei, Jiang Xing-Hua
Department of Anesthesiology, the Second Xiangya Hospital of Central South University, Changsha, Hunan Province, China.
Neural Regen Res. 2015 May;10(5):772-7. doi: 10.4103/1673-5374.156979.
Previous studies have shown that microglia impact the proliferation and differentiation of neurons during hippocampal neurogenesis via the fractalkine/CX3 chemokine receptor 1 (CX3CR1) signaling pathway. However, whether microglia can influence the maturation and dendritic growth of newborn neurons during hippocampal neurogenesis remains unclear. In the present study, we found that the number of doublecortin-positive cells in the hippocampus was decreased, and the dendritic length and number of intersections in newborn neurons in the hippocampus were reduced in transgenic adult mice with CX3CR1 deficiency (CX3CR1 (GFP/GFP) ). Furthermore, after experimental seizures were induced with kainic acid in these CX3CR1-deficient mice, the expression of c-fos, a marker of neuronal activity, was reduced compared with wild-type mice. Collectively, the experimental findings indicate that the functional maturation of newborn neurons during hippocampal neurogenesis in adult mice is delayed by CX3CR1 deficiency.
先前的研究表明，小胶质细胞在海马神经发生过程中通过趋化因子/ CX3趋化因子受体1（CX3CR1）信号通路影响神经元的增殖和分化。然而，小胶质细胞在海马神经发生过程中是否能影响新生神经元的成熟和树突生长仍不清楚。在本研究中，我们发现CX3CR1缺陷的转基因成年小鼠（CX3CR1 (GFP/GFP) ）海马中双皮质素阳性细胞数量减少，海马新生神经元的树突长度和交叉点数量减少。此外，在用海藻酸诱导这些CX3CR1缺陷小鼠发生实验性癫痫发作后，与野生型小鼠相比，神经元活性标志物c-fos的表达降低。总体而言，实验结果表明，CX3CR1缺陷会延迟成年小鼠海马神经发生过程中新生神经元的功能成熟。
