β淀粉样蛋白肽诱导的前额叶皮层活动变化及其对海马输入的反应

Ernesto Flores-Martínez, F. Peña-Ortega
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引用次数: 20

摘要

前额皮质(PFC)功能的改变及其与其他大脑区域(即海马体)相互作用的异常与阿尔茨海默病(AD)有关。考虑到这些功能障碍与大脑淀粉样蛋白β (a β)肽产生的增加相关,我们在这里寻找AD的这些病理征候之间的因果关系。因此,我们在体外测试了Aβ是否通过海马输入刺激影响PFC网络的活性和该皮层的激活。我们发现,当海马输入受到刺激时,在群体和单细胞水平上,将Aβ应用于脑切片可抑制PFC自发网络活动以及PFC激活。我们的数据表明,Aβ可以通过破坏PFC活动及其在整个大脑中的远程相互作用来促进AD。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Amyloid β Peptide-Induced Changes in Prefrontal Cortex Activity and Its Response to Hippocampal Input
Alterations in prefrontal cortex (PFC) function and abnormalities in its interactions with other brain areas (i.e., the hippocampus) have been related to Alzheimer Disease (AD). Considering that these malfunctions correlate with the increase in the brain's amyloid beta (Aβ) peptide production, here we looked for a causal relationship between these pathognomonic signs of AD. Thus, we tested whether or not Aβ affects the activity of the PFC network and the activation of this cortex by hippocampal input stimulation in vitro. We found that Aβ application to brain slices inhibits PFC spontaneous network activity as well as PFC activation, both at the population and at the single-cell level, when the hippocampal input is stimulated. Our data suggest that Aβ can contribute to AD by disrupting PFC activity and its long-range interactions throughout the brain.
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