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首页> 外文期刊>The European Journal of Neuroscience >Enhanced cell death in hippocampus and emergence of cognitive impairments following a localized mini-stroke in hippocampus if preceded by a previous episode of acute stress.
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Enhanced cell death in hippocampus and emergence of cognitive impairments following a localized mini-stroke in hippocampus if preceded by a previous episode of acute stress.

机译：如果先前有急性应激发作，海马局部小中风后海马的细胞死亡增加和认知障碍的出现。

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This series of experiments represents a test of a theory concerning the etiology of age-related cognitive decline, including Alzheimer's disease (AD). The theory suggests that multiple combinations of cofactors produce variants of these disorders. Two factors that have been linked to the etiology of AD, that are of interest to our laboratories, are stress and vascular strokes. The current experiments tested the cofactors theory by evaluating the neuronal and functional effects of localized subthreshold strokes in the hippocampus of different groups of rats. One group experienced episodes of stress prior to stroke induction while the other did not. The results showed that a low dose of endothelin-1 (ET-1) injected into the hippocampus of groups of rats that had previously experienced stressful episodes showed enhanced hippocampal cell death and neurodegeneration that did not occur in the rats that did not experience stress prior to stroke induction. The results also showed that the stressed rats given subthreshold ET-1 injections into the hippocampus showed hippocampal-based learning and memory deficits that were not present in the non-stressed group given the same injections. This pattern of results suggests that individuals that are under stress are more vulnerable to insults to the hippocampus that have little effect on an individual that is not stressed. This vulnerability might be due to the actions of stress hormones, like the glucocorticoids, that have been previously shown to endanger hippocampal neurons.
机译：这一系列实验代表了有关与年龄相关的认知功能下降（包括阿尔茨海默氏病（AD））的病因的理论的测试。该理论表明，辅助因子的多种组合会产生这些疾病的变异。我们实验室感兴趣的与AD病因相关的两个因素是压力和血管性中风。当前的实验通过评估不同组大鼠海马中局部亚阈下中风的神经元和功能作用，测试了辅助因子理论。一组在中风诱发之前经历了压力发作，而另一组则没有。结果表明，向先前经历过应激发作的各组大鼠海马中注射低剂量的内皮素-1（ET-1），其海马细胞死亡和神经退行性疾病的发生率增加，而之前未经历过应激的大鼠则没有这种现象中风诱导。结果还表明，给海马亚阈值ET-1注射的压力大鼠表现出基于海马的学习和记忆障碍，而在相同压力下非受压组则没有这种情况。这种结果模式表明，处于压力下的人更容易受到海马的侮辱，而对没有受到压力的人几乎没有影响。此漏洞可能是由于压力激素（如糖皮质激素）的作用引起的，以前已经证明它们会危害海马神经元。

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