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神经元细胞膜的电生理损伤改变了电突触的同步化。

Electrophysiological damage to neuronal membrane alters ephaptic entrainment.

机构信息

Departamento de Física Teórica e Experimental, Universidade Federal do Rio Grande do Norte, Natal, RN, 59078-970, Brazil.

Departamento de Biofísica e Farmacologia, Universidade Federal do Rio Grande do Norte, Natal, RN, 59078-970, Brazil.

出版信息

Sci Rep. 2023 Jul 24;13(1):11974. doi: 10.1038/s41598-023-38738-x.

DOI:10.1038/s41598-023-38738-x
PMID:37488148
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10366241/
Abstract

The brain is commonly understood as a complex network system with a particular organization and topology that can result in specific electrophysiological patterns. Among all the dynamic elements resulting from the circuits of the brain's network, ephapticity is a cellular communication mechanism that has received little attention. To understand the network's properties of ephaptic entrainment, we start investigating the ephaptic effect on a single neuron. In this study, we used numerical simulations to examine the relationship between alterations in ephaptic neuronal entrainment and impaired electrophysiological properties of the neuronal membrane, which can occur via spike field coherence (SFC). This change in frequency band amplitude is observed in some neurodegenerative diseases, such as Parkinson's or Alzheimer's. To further investigate these phenomena, we proposed a damaged model based on the impairment of both the resistance of the ion channels and the capacitance of the lipid membrane. Therefore, we simulated ephaptic entrainment with the hybrid neural model quadratic integrate-and-fire ephaptic (QIF-E), which mimics an ephaptic entrainment generated by an LFP (simulate a neuronal group). Our results indicate a link between peak entrainment (ephapticity) preference and a shift in frequency band when damage occurs mainly in ion channels. Finally, we discuss possible relationships between ephaptic entrainment and neurodegenerative diseases associated with aging factors.

摘要

大脑通常被理解为具有特定组织和拓扑结构的复杂网络系统,这可能导致特定的电生理模式。在大脑网络电路产生的所有动态元素中,电突触是一种细胞通讯机制,它受到的关注较少。为了了解网络的电突触同步特性,我们首先研究电突触对单个神经元的影响。在这项研究中,我们使用数值模拟来检查电突触神经元同步变化与神经元膜电生理性质受损之间的关系,这种变化可能通过尖峰场相干(SFC)发生。这种频带幅度的变化在一些神经退行性疾病中观察到,如帕金森病或阿尔茨海默病。为了进一步研究这些现象,我们提出了一个基于离子通道电阻和脂质膜电容受损的损伤模型。因此,我们使用混合神经模型二次积分和放电电突触(QIF-E)模拟电突触同步,该模型模拟由 LFP 产生的电突触同步(模拟神经元群)。我们的结果表明,在主要发生在离子通道的损伤时,峰同步(电突触性)偏好与频带移位之间存在联系。最后,我们讨论了电突触同步与与衰老因素相关的神经退行性疾病之间的可能关系。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3947/10366241/73b1b2ea7a83/41598_2023_38738_Fig7_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3947/10366241/134f2c368452/41598_2023_38738_Fig1_HTML.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3947/10366241/017a5e4c7a01/41598_2023_38738_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3947/10366241/e1cf726968f1/41598_2023_38738_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3947/10366241/79448e4c3444/41598_2023_38738_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3947/10366241/73b1b2ea7a83/41598_2023_38738_Fig7_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3947/10366241/134f2c368452/41598_2023_38738_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3947/10366241/957696723966/41598_2023_38738_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3947/10366241/fd2373525d72/41598_2023_38738_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3947/10366241/017a5e4c7a01/41598_2023_38738_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3947/10366241/e1cf726968f1/41598_2023_38738_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3947/10366241/79448e4c3444/41598_2023_38738_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3947/10366241/73b1b2ea7a83/41598_2023_38738_Fig7_HTML.jpg

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Nature. 2021 Mar;591(7850):431-437. doi: 10.1038/s41586-021-03185-z. Epub 2021 Jan 27.
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Disruption of neocortical synchronisation during slow-wave sleep in the rotenone model of Parkinson's disease.帕金森病鱼藤酮模型中慢波睡眠期间新皮层同步的破坏。
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