海马异常成体神经发生所致的局部兴奋性神经环路形成是导致癫癎发生、发展的重要原因之一。趋化因子受体CXCR7参与并调控海马齿状回的成体神经发生，其异常表达将会导致齿状回颗粒细胞的成体神经发生出现异常，进而引起颗粒细胞兴奋性增高，促进海马齿状回-CA3兴奋性神经环路的形成。因此，我们推测CXCR7通过调控海马齿状回的成体神经发生，进而参与癫癎的形成。我们前期的研究已经发现，CXCR7在小鼠癫癎模型的齿状回与颞叶癫癎患者的脑组织中均出现了表达的上调，但是CXCR7的异常表达是否可以通过促进齿状回颗粒细胞的异常成体神经发生进而参与癫癎的形成还不得而知。本项目拟通过基因沉默与过表达技术干预CXCR7在齿状回的表达，并结合Q-tracker标记追踪技术、膜片钳技术、在体多通道场电位记录等实验手段，从成体神经发生的层面来探讨CXCR7在癫癎形成中的作用与机制，为癫癎发病机制的研究提供新的思路与实验依据。

Hyperexcitability in hippocampal circuits caused by aberrant hippocampal adult neurogenesis is one of the crucial reasons for epilepsy. CXCR7 can regulate the adult neurogenesis in hippocampal dentate gyrus (DG). Abnormal expression of CXCR7 will result in aberrant adult neurogenesis in hippocampal DG, which leads to hyperexcitability of hippocampal granular cells and abnormal neural pathway from DG to CA3, and then contributes to hippocampal hyperexcitability circuits. Therefore, we assumed that CXCR7 may participate in epileptogenesis through regulating hippocampal DG adult neurogenesis. Our previous study has showed that the expression of CXCR7 was up-regulated in both DG of epileptic mouse model and brain tissues of epileptic patients; however, the underlying function and molecular mechanism of CXCR7 regulating hippocampal dentate gyrus adult neurogenesis in epilepsy remain unknown. Therefore, we aim to explore and investigate the role and mechanism of CXCR7 in aberrant hippocampal adult neurogenesis of epilepsy by knockdown and over-expression of CXCR7 in hippocampal DG combined with Q-tracker labeling and tracking technique, patch-clamp recording, multielectrode local field potential recording in vivo and other research methods, thereby providing fresh ideas and laboratory basis for the mechanism of epileptogenesis.