Bai Wenwen, Yi Hu, Liu Tiaotiao, Wei Jing, Tian Xin
Department of Biomedical Engineering, School of Biomedical Engineering and Technology, Tianjin Medical University Tianjin, China.
Front Behav Neurosci. 2014 Nov 27;8:411. doi: 10.3389/fnbeh.2014.00411. eCollection 2014.
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.
阿尔茨海默病（AD）是一种逐渐导致认知缺陷的神经退行性疾病。工作记忆受损在AD中较为常见。众所周知，峰电位和局部场电位（LFP）以及它们之间的协同作用在正常脑功能中编码信息。然而，AD认知缺陷中峰电位与LFP之间的异常协同作用在很大程度上仍未得到充分研究。由于β淀粉样肽（Aβ）是AD认知障碍的致病因素，深入了解Aβ对认知障碍的作用机制可能为AD的病理生理学提供重要见解。在本研究中，我们同时记录了植入大鼠前额叶皮层（对照组和海马内注射Aβ组）的多个电极的峰电位和LFP，这些大鼠执行Y迷宫工作记忆任务。通过计算熵来评估任务期间峰电位和LFP的信息变化。然后通过LFP熵和峰电位熵的相关性来估计峰电位和LFP之间的协同作用。与对照组相比，Aβ组峰电位和LFP之间的协同作用明显较弱。我们的结果表明，峰电位和LFP之间的不协调可能是AD工作记忆认知缺陷的潜在机制。
