PI3K/AKT/GSK3β/CRMP-2-mediated neuroplasticity in depression induced by stress.
PI3K/AKT/GSK3β/CRMP-2-mediated neuroplasticity in depression induced by stress.
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DOI：
10.1097/wnr.0000000000001096
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发表时间：
2018-10
期刊：
影响因子：
1.7
通讯作者：
Zuotian Wu;Gaohua Wang;Yanyan Wei;L. Xiao;Hui-ling Wang
中科院分区：
文献类型：
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作者：
Zuotian Wu;Gaohua Wang;Yanyan Wei;L. Xiao;Hui-ling Wang
早期神经发育不良或紊乱是抑郁症的重要刺激因素，但早期应激容易损害神经发育，导致神经可塑性降低。由于神经细胞、神经环路、结构不稳定等特点，应激往往会导致抑郁症的发生和复发。应激通常与中枢神经系统中炎症因子的释放有关。最近的研究表明，神经炎性因子最有可能参与应激性抑郁的发生和发展，通过中枢炎症因子攻击神经细胞。神经可塑性的改变，如神经支架的微管系统、轴突的伸展、神经接头的再生、神经递质的合成、传递和释放的障碍以及突触的异常，都会导致神经细胞之间的信息传递异常，从而导致抑郁症状。神经支架微管结构的改变与应激性抑郁症的神经可塑性损害密切相关。我们以前的研究和目前的研究都发现，AKT/GSK3CRMP-2通路介导了神经支架微管可塑性的变化。中枢性炎症因子与这一途径之间存在相互作用。因此，从神经炎损伤和神经支架可塑性变化的角度，可以推断，在应激状态下中枢炎性因子被激活和释放后，其可能的机制是通过改变中枢神经细胞支架微管系统的正常结构和功能，通过Akt/Gsk3β/CRMP-2通路介导的。
Early neurodevelopmental dysplasia or disorder is an important stimulus for depression, but early stress can easily damage nerve development and lead to decreased neural plasticity. Because of the characteristics of nerve cell, nerve loop, structure instability and so on, stress can often lead to the occurrence and recurrence of depression. Stress is often associated with the release of inflammatory factors in the central nervous system. Recent studies suggest that neuroinflammatory factors are most likely involved in the occurrence and development of stress-induced depression, attacking neuronal cells through central inflammatory factors. The changes in neural plasticity, such as microtubule system of nerve scaffold, extension of axonal dendrites, regeneration of nerve junctions, disturbance of neurotransmitter synthesis, transmission and release, and abnormal synapses, cause abnormal transmission of information between nerve cells and cause symptoms of depression. The changes in the structure of neural stent microtubules are closely related to the neuroplastic damage of depression induced by stress. Our previous studies and current studies have found that the AKT/GSK3β/CRMP-2 pathway mediates the changes in neural stent microtubule plasticity. There is an interaction between central inflammatory factors and this pathway. Therefore, from the point of view of neuritis injury and the plasticity change of nerve scaffold, it can be concluded that after the activation and release of central inflammatory factor under stress, the possible mechanism of depression is mediated by the AKT/GSK3β/CRMP-2 pathway by changing the normal structure and function of the central nervous cell scaffold microtubule system.