癫痫被认为是中枢神经环路发育异常的严重神经类疾病。皮层中间神经元发育或功能异常引起皮层兴奋性-抑制性失衡被认为是癫痫核心病理机制之一。前期研究表明，ALG13可能是人类癫痫发生的易感基因。然而，其突变导致癫痫的病理机制并不清楚。因此，我们利用敲除Alg13的小鼠模型，结合分子生物学、生物信息学等技术，从细胞、环路、系统和整体等多水平，来研究在小鼠胚胎期和后天发育中Alg13的时空表达，Alg13缺失对中间神经元皮层分布和数量、分化和切线迁移、神经元树突发育、迁移导向因子、腹侧端脑区域化模式形成及相关转录因子的影响，从而探究Alg13对皮层中间神经元发育的影响及该基因的缺失造成异常发育的神经环路从而导致癫痫发病的潜在机制。我们的研究将有助于理解中间神经元发育的分子调控机理，从而进一步探究由中间神经元异常引起的神经精神类疾病的致病机制。

Epilepsy is known as a serious neurological disease with the abnormal development of the central nervous circuit. The cortical excitatory-inhibitory imbalance caused by the abnormal development or function of cortical interneurons is considered to be one of the key pathological mechanisms of the epilepsy. Previous studies have shown that ALG13 may be a susceptible gene for human epilepsy. However, the pathogenesis of its mutation leading to epilepsy is not clear. Therefore, we use the Alg13 knockout mouse model, combined with molecular biology, bioinformatics and other technologies, to study the time and space specificity of Alg13 expression in the embryonic stage and after birth; to explore the effect of Alg13 deletion on the cortical distribution, number, differentiation and tangential migration of interneurons, the neuronal dendrite development, migration-directing factors, the formation of ventral brain regionalization pattern and related transcription factors. From multiple levels of cells, circuits, systems and wholes, we may investigate the role of Alg13 on the influence of cortical interneuron development and the underlying mechanism of epilepsy caused by an abnormally developed neural circuit due to a lack of this gene. Our research will help to understand the molecular regulation mechanism of the development of interneurons, and further explore the pathogenic mechanism of neuropsychiatric diseases caused by the abnormality of interneurons.