PDF(Pubmed)
Abstract：
The present study utilized the spared nerve injury (SNI) to create a mouse model of depression to investigate the impact of esketamine on depressive-like behaviors, on the expression of PSD-95 and CRMP2 proteins, and on changes in neuronal dendritic spine plasticity in the prefrontal cortex (PFC). Depressive-like behavioral tests were performed 1 h after esketamine treatment, and the PFC tissues were obtained on the fourth day after completing the behavioral tests. Then, dendritic spine density and morphology in the PFC were measured using Golgi staining, and CRMP2 and PSD-95 proteins were obtained from PFC tissue by western blotting. The results of this study showed that esketamine significantly increased the immobility time in the forced swimming test and tail suspension test. In the open field test, esketamine increased the time spent in the open arms, the time spent in the central area, and the total distance covered. It also increased the protein expression levels of CRMP2 and PSD-95 in addition to the total and mature dendritic spine density of the PFC in SNI-depressed mice. Esketamine can significantly improve depression-like behaviors in SNI-depressed mice and promote an increase in dendritic spine density and maturation in the PFC. These effects may be associated with changes in CRMP2 and PSD-95 expression.
摘要：
本研究利用备用神经损伤（SNI）创建抑郁症小鼠模型，以研究艾氯胺酮对抑郁样行为的影响，PSD-95和CRMP2蛋白的表达，以及前额叶皮质（PFC）中神经元树突棘可塑性的变化。在艾氯胺酮治疗后1小时进行抑郁样行为测试，并且在完成行为测试后的第四天获得PFC组织。然后，使用高尔基染色测量PFC中的树突棘密度和形态，通过蛋白质印迹从PFC组织中获得CRMP2和PSD-95蛋白。这项研究的结果表明，在强迫游泳试验和悬尾试验中，艾氯胺酮显着增加了不动时间。在野外测试中，艾氯胺酮增加了张开双臂的时间，在中心地区度过的时间，和覆盖的总距离。除了SNI抑郁小鼠中PFC的总和成熟树突棘密度外，它还增加了CRMP2和PSD-95的蛋白质表达水平。Esketamine可以显着改善SNI抑郁小鼠的抑郁样行为，并促进PFC中树突棘密度和成熟的增加。这些效应可能与CRMP2和PSD-95表达的变化有关。
