关键词: NECL4, 树突棘, CaMKIIα, CDC42, ERK

Abstract: Objective To investigate the effect of synaptic adhesion molecule nectin-like molecule 4 (NECL4) on Ca²⁺-CaMKII-CDC42 signal pathway and the number of dendritic spines. Methods Using Necl4 knockout mice as the research animal, the brain tissues of 8-week-old Necl4 wild type (WT) and knockout (KO) mice were stained with Golgi staining, then the density of dendritic spines on the secondary dendrites in layer Ⅱ/Ⅲ of cerebral cortex neuron was examined. Western blot and RT-qPCR were used to detect the protein and mRNA expression of Ca²⁺-CaMKII signal pathway and downstream signal molecules, including CDC42, Rac1, RhoA, H-Ras, ERK and other signal proteins. Results The Golgi staining showed that the number of dendritic spines on the secondary dendrites of the cerebral cortex Ⅱ/Ⅲ layer neuron in Necl4 knockout mice was less than that in wild type mice(P＜0.01). The results of Western blot showed that the expression of CaMKIIα (P＜0.05) and phospho-CaMKIIα (Thr286) (P＜0.05) decreased in Necl4 knockout mice. The mRNA (P＜0.05) and protein (P＜0.05) levels of CDC42 were decreased in Necl4 knockout mice. Conclusions NECL4 regulates the number of dendritic spines in mouse cerebral cortex through Ca²⁺-CaMKII-CDC42 signal pathway.

Key words: NECL4, dendritic spine, CaMKIIα, CDC42, ERK