首页> 外文期刊>Neurochemistry International: The International Journal for the Rapid Publication of Critical Reviews, Preliminary and Original Research Communications in Neurochemistry >Cdh1 overexpression improves emotion and cognitive-related behaviors via regulating hippocampal neuroplasticity in global cerebral ischemia rats
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Cdh1 overexpression improves emotion and cognitive-related behaviors via regulating hippocampal neuroplasticity in global cerebral ischemia rats

机译:CDH1过表达通过调节全球脑缺血大鼠的海马神经塑性来改善情绪和认知相关行为

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摘要

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 Cdhi overexpression exerts a neuroprotective effect by regulating hippocampal neuroplasticity thus improving negative emotionality and cognitive deficits after tGCI/R.
机译:行程后幸存者表现出认知赤字并进行情绪损害。然而,全球脑缺血对情绪和潜在机制的标准行为措施的影响仍然很大程度上是未知的。我们以前的工作发现CDH1的下调有助于大鼠的缺血性神经元死亡,因此我们假设CDH1在脑缺血后发挥在情感态度中的作用,我们研究了CDH1过表达对神经发生行为的影响和瞬态全球脑中的可能机制缺血再灌注(TGCI / R)大鼠。使用一系列行为测试来评估情感和认知相关行为,并且使用分子生物学技术来研究海马神经塑性。结果表明,TGCI / R大鼠显示出焦虑和抑郁症的行为和一定程度的认知障碍,并且这些异常行为伴随着海马突触和树突脊柱的丧失,树突中的破坏以及间隙水平的下降-43,Synaptophysin,Synapsin和PSD-95。然而,CDH1过表达改善了负性情绪,改善认知缺陷,拯救海马突触损失,预防树突网络紊乱,并在TGCI / R后增加了突触相关蛋白的水平。在一起,这些发现表明CDHI过表达通过调节海马神经塑性,从而提高TGCI / R后的阴性情绪和认知缺陷施加神经保护作用。

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