淀粉样β肽在体外对海马θ节律有不同影响。

International Journal of Peptides Pub Date : 2013-01-01 Epub Date: 2013-06-25 DOI:10.1155/2013/328140
Armando I Gutiérrez-Lerma, Benito Ordaz, Fernando Peña-Ortega
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引用次数: 25

摘要

可溶性淀粉样蛋白β肽(A β)与阿尔茨海默病早期认知功能障碍有关。胆碱能和谷氨酸能诱导的海马θ节律都与学习记忆、空间导航和空间记忆有关。然而,这两种节律并不完全相同;它们与不同的行为相关联,可以通过不同的实验条件进行差异调节。因此,在本研究中,我们的目的是研究可溶性A β的应用是否会改变胆碱能和谷氨酸能激动剂碳醇或DHPG分别在大鼠海马切片中产生的两种频率振荡网络活动。由于已有证据表明不同的Aβ肽对振荡活性有不同的影响,我们还比较了Aβ 25-35和Aβ 1-42在相同浓度(0.5 ~ 1.0 μ M)下对体外θ节律的影响,发现Aβ 25-35降低了碳甾醇诱导的群体θ振荡活性,但效力低于Aβ 1-42。相比之下,高浓度的a β 25-35不影响dhpg诱导的振荡活性,但a β 1-42降低了dhpg诱导的振荡活性。我们的研究结果支持这样一种观点,即不同的淀粉样肽可能改变与特定神经网络活动产生相关的特定细胞机制,而不是对神经网络功能产生普遍的抑制作用。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

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Amyloid Beta peptides differentially affect hippocampal theta rhythms in vitro.

Soluble amyloid beta peptide (A β ) is responsible for the early cognitive dysfunction observed in Alzheimer's disease. Both cholinergically and glutamatergically induced hippocampal theta rhythms are related to learning and memory, spatial navigation, and spatial memory. However, these two types of theta rhythms are not identical; they are associated with different behaviors and can be differentially modulated by diverse experimental conditions. Therefore, in this study, we aimed to investigate whether or not application of soluble A β alters the two types of theta frequency oscillatory network activity generated in rat hippocampal slices by application of the cholinergic and glutamatergic agonists carbachol or DHPG, respectively. Due to previous evidence that oscillatory activity can be differentially affected by different A β peptides, we also compared Aβ 25-35 and Aβ 1-42 for their effects on theta rhythms in vitro at similar concentrations (0.5 to 1.0  μ M). We found that Aβ 25-35 reduces, with less potency than Aβ 1-42, carbachol-induced population theta oscillatory activity. In contrast, DHPG-induced oscillatory activity was not affected by a high concentration of Aβ 25-35 but was reduced by Aβ 1-42. Our results support the idea that different amyloid peptides might alter specific cellular mechanisms related to the generation of specific neuronal network activities, instead of exerting a generalized inhibitory effect on neuronal network function.

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