Incoordination between spikes and LFPs in Aβ1-42-mediated memory deficits in rats.
Incoordination between spikes and LFPs in Aβ1-42-mediated memory deficits in rats.
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A beta(1-42) 介导的大鼠记忆缺陷中尖峰和 LFP 之间的不协调
DOI：
10.3389/fnbeh.2014.00411
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发表时间：
2014
影响因子：
3
通讯作者：
Tian X
中科院分区：
文献类型：
--
作者：
Bai W;Yi H;Liu T;Wei J;Tian X
阿尔茨海默病（Alzheimer's disease，AD）是一种逐渐引起认知功能障碍的神经退行性疾病。工作记忆的损害通常在AD中观察到。在正常的脑功能中，棘波和局部场电位（LFP）以及它们之间的协调编码信息。然而，在AD的认知缺陷的尖峰和LFPs之间的异常协调仍然在很大程度上未被探索。由于淀粉样β肽（Aβ）是AD认知障碍的致病因子，因此，深入了解Aβ在AD认知障碍中的作用机制可能有助于深入了解AD的病理生理机制。在本研究中，我们同时记录了多个电极植入大鼠（对照组和海马内Aβ注射组）的前额叶皮层的棘波和LFPs，执行Y-迷宫工作记忆任务。通过熵的计算来评估作业过程中锋电位和LFPs的信息变化。然后通过LFP熵和锋电位熵的相关性来估计锋电位和LFP之间的协调性。与对照组相比，Aβ组的棘波与LFPs之间的协调性明显减弱。我们的研究结果表明，棘波和LFPs之间的不协调可能提供了一个潜在的机制，在AD的工作记忆的认知缺陷。
Alzheimer's disease (AD) is a neurodegenerative disease that gradually induces cognitive deficits. Impairments of working memory have been typically observed in AD. It is well known that spikes and local field potentials (LFPs) as well as the coordination between them encode information in normal brain function. However, the abnormal coordination between spikes and LFPs in the cognitive deficits of AD has remained largely unexplored. As amyloid-β peptide (Aβ) is a causative factor for the cognitive impairments of AD, developing a mechanistic understanding of the contribution of Aβ to cognitive impairments may yield important insights into the pathophysiology of AD. In the present study, we simultaneously recorded spikes and LFPs from multiple electrodes implanted in the prefrontal cortex of rats (control and intra-hippocampal Aβ injection group) that performed a Y-maze working memory task. The information changes in spikes and LFPs during the task were assessed by calculation of entropy. Then the coordination between spikes and LFPs was estimated by the correlation of LFP entropy and spike entropy. Compared with the control group, the Aβ group showed significantly weaker coordination between spikes and LFPs. Our results indicate that the incoordination between spikes and LFPs may provide a potential mechanism for the cognitive deficits in working memory of AD.
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影响因子：
5.7
作者：
Gordon JA
通讯作者：
Gordon JA
DOI：
10.1590/s0100-879x2000000900002
发表时间：
2000-09-01
影响因子：
2.3
作者：
Baddeley, A;Bueno, O;Da Cunha, C
通讯作者：
Da Cunha, C
影响因子：
5.7
作者：
Dauwels, J.;Vialatte, F.;Cichocki, A.
通讯作者：
Cichocki, A.
影响因子：
34.7
作者：
Hikosaka, Okihide
通讯作者：
Hikosaka, Okihide
影响因子：
14.5
作者：
BADDELEY, AD;BRESSI, S;SPINNLER, H
通讯作者：
SPINNLER, H