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Cdh1 overexpression improves emotion and cognitive-related behaviors via regulating hippocampal neuroplasticity in global cerebral ischemia rats.
Neurochemistry international ( IF 4.2 ) Pub Date : 2019-01-21 , DOI: 10.1016/j.neuint.2019.01.015
Bo Zhang 1 , Xuhui Chen 2 , Youyou Lv 3 , Xi Wu 1 , Lingli Gui 2 , Yue Zhang 2 , Jin Qiu 2 , Guizhi Song 4 , Wenlong Yao 2 , Li Wan 2 , Chuanhan Zhang 2
Affiliation  

Post-stroke survivors exhibited cognitive deficits and performed emotional impairment. However, the effect of global cerebral ischemia on standard behavioral measures of emotionality and underlying mechanism remain largely unknown. Our previous work identified that down-regulation of Cdh1 contributed to ischemic neuronal death in rat, thus we hypothesized that Cdh1 exerts a role in emotionality after cerebral ischemia, and we investigated the effect of Cdh1 overexpression on neurogenic behaviors and possible mechanisms in transient global cerebral ischemia reperfusion (tGCI/R) rats. A series of behavioral tests were used to evaluate emotion and cognitive related behaviors, and molecular biological techniques were employed to investigate hippocampal neuroplasticity. The results showed that tGCI/R rats displayed anxiety- and depression-like behaviors and a certain degree of cognitive impairment, and these abnormal behaviors accompanied with a loss of hippocampal synapses and dendritic spines, disruption of dendrite arborization and decline in the level of GAP-43, synaptophysin, synapsin and PSD-95. However, Cdh1 overexpression improved negative emotionality, ameliorated cognitive deficits, rescued hippocampal synapses loss, prevented dendritic network disorganization, and increased the level of synaptic-associated proteins after tGCI/R. Taken together, these findings suggest that Cdh1 overexpression exerts a neuroprotective effect by regulating hippocampal neuroplasticity thus improving negative emotionality and cognitive deficits after tGCI/R.

中文翻译:

Cdh1过表达通过调节全脑缺血大鼠的海马神经可塑性来改善情绪和认知相关行为。

中风后幸存者表现出认知缺陷并表现出情绪障碍。然而,全球性脑缺血对情绪行为和潜在机制的标准行为测量的影响仍然未知。我们以前的工作发现,Cdh1的下调会导致大鼠缺血性神经元死亡,因此我们假设Cdh1在脑缺血后的情绪中发挥作用,并研究了Cdh1过表达对短暂性全脑性神经元行为和可能机制的影响。缺血再灌注(tGCI / R)大鼠。使用一系列行为测试来评估情绪和认知相关行为,并使用分子生物学技术研究海马神经可塑性。结果表明,tGCI / R大鼠表现出焦虑和抑郁样行为,并有一定程度的认知障碍,这些异常行为伴有海马突触和树突棘的丧失,树突状乔木的破坏和GAP水平的下降。 -43,突触素,突触素和PSD-95。然而,Cdh1过表达改善了负面情绪,减轻了认知缺陷,挽救了海马突触的丢失,防止了树突状网络的混乱,并增加了tGCI / R后突触相关蛋白的水平。综上所述,这些发现表明Cdh1过表达通过调节海马神经可塑性来发挥神经保护作用,从而改善tGCI / R后的负面情绪和认知缺陷。这些异常行为伴有海马突触和树突棘的丧失,树突状树突的破坏以及GAP-43,突触素,突触素和PSD-95的水平下降。然而,Cdh1过表达改善了负面情绪,减轻了认知缺陷,挽救了海马突触的丢失,防止了树突状网络的混乱,并增加了tGCI / R后突触相关蛋白的水平。综上所述,这些发现表明Cdh1过表达通过调节海马神经可塑性来发挥神经保护作用,从而改善tGCI / R后的负面情绪和认知缺陷。这些异常行为伴有海马突触和树突棘的丧失,树突状树突的破坏以及GAP-43,突触素,突触素和PSD-95的水平下降。然而,Cdh1过表达改善了负面情绪,减轻了认知缺陷,挽救了海马突触的丢失,防止了树突状网络的混乱,并增加了tGCI / R后突触相关蛋白的水平。综上所述,这些发现表明Cdh1过表达通过调节海马神经可塑性来发挥神经保护作用,从而改善tGCI / R后的负面情绪和认知缺陷。Cdh1过表达改善了负面情绪,减轻了认知缺陷,挽救了海马突触的丢失,防止了树突状网络的混乱,并增加了tGCI / R后突触相关蛋白的水平。综上,这些发现表明Cdh1过表达通过调节海马神经可塑性来发挥神经保护作用,从而改善tGCI / R后的负面情绪和认知缺陷。Cdh1过表达改善了负面情绪,减轻了认知缺陷,挽救了海马突触的丢失,防止了树突状网络的混乱,并增加了tGCI / R后突触相关蛋白的水平。综上所述,这些发现表明Cdh1过表达通过调节海马神经可塑性来发挥神经保护作用,从而改善tGCI / R后的负面情绪和认知缺陷。
更新日期:2019-01-21
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