Objective To study the expression of REST in corticosterone model mice and the effect of REST expression on depression and anxiety behavior in mice, and to explore its role in the mouse model of depression.
Methods A mouse model of chronic stress was established by repeated subcutaneous injection of corticosterone, and AAV virus vector was used to overexpress REST in the mouse brain. The changes of depression and anxiety phenotype in mice were detected behaviorally, and real-time quantitative PCR was used to explore the effect of REST on related genes. .
Results Repeated subcutaneous injection of corticosterone for 4 weeks could significantly reduce the body weight of mice (P < 0.01) and induce depression-like behaviors in mice. Overexpression of REST in the hippocampus affects the performance of model mice in behavioral tests of depression and anxiety, alleviates the depression-like phenotype, and reduces the immobility time of model mice in the tail suspension test and forced swimming test; induces anxiety symptoms, enters the open space The number of times in the central area of the field decreased, and the number of explorations and the dwell time of the closed arms of the elevated plus maze increased; meanwhile, the RNA transcription levels of Bndf, Nt3, Ngf, and Fgf2 could be regulated.
Conclusion REST plays a two-way regulatory role in the corticosterone stress depression model, not a single depressive behavior, and its mechanism may be related to the comprehensive effect of multiple genes and signaling pathways involved in regulating expression.