Ma Ke, Guo Li, Xu Aiping, Cui Shan, Wang Jin-Hui
Qingdao University, School of Pharmacy, Shandong, China.
State Key Lab of Brain and Cognitive Science, Institute of Biophysics, Chinese Academy of Sciences, Beijing, China.
PLoS One. 2016 Jul 18;11(7):e0159093. doi: 10.1371/journal.pone.0159093. eCollection 2016.
Major depression is a prevalent mood disorder. Chronic stress is presumably main etiology that leads to the neuron and synapse atrophies in the limbic system. However, the intermediate molecules from stresses to neuronal atrophy remain elusive, which we have studied in the medial prefrontal cortices from depression mice.
The mice were treated by the chronic unpredictable mild stress (CUMS) until they expressed depression-like behaviors confirmed by the tests of sucrose preference, forced swimming and Y-maze. High-throughput sequencings of microRNA and mRNA in the medial prefrontal cortices were performed in CUMS-induced depression mice versus control mice to demonstrate the molecular profiles of major depression. In the medial prefrontal cortices of depression-like mice, the levels of mRNAs that translated the proteins for the GABAergic synapses, dopaminergic synapses, myelination, synaptic vesicle cycle and neuronal growth were downregulated. miRNAs of regulating these mRNAs are upregulated.
The deteriorations of GABAergic and dopaminergic synapses as well as axonal growth are associated with CUMS-induced depression.
重度抑郁症是一种常见的情绪障碍。慢性应激可能是导致边缘系统神经元和突触萎缩的主要病因。然而，从应激到神经元萎缩的中间分子仍不清楚，我们在抑郁症小鼠的内侧前额叶皮质中对此进行了研究。
通过慢性不可预测轻度应激（CUMS）处理小鼠，直至通过蔗糖偏好试验、强迫游泳试验和Y迷宫试验确认它们表现出类似抑郁的行为。对CUMS诱导的抑郁症小鼠与对照小鼠的内侧前额叶皮质进行微小RNA和信使核糖核酸的高通量测序，以展示重度抑郁症的分子特征。在表现出类似抑郁症状的小鼠的内侧前额叶皮质中，与γ-氨基丁酸能突触、多巴胺能突触、髓鞘形成、突触小泡循环和神经元生长相关的蛋白质的信使核糖核酸水平下调。调节这些信使核糖核酸的微小RNA上调。
γ-氨基丁酸能和多巴胺能突触的退化以及轴突生长与CUMS诱导的抑郁症有关。
