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钾离子浓度对海马体耦合神经元模型中癫痫发作的影响。

The influence of potassium concentration on epileptic seizures in a coupled neuronal model in the hippocampus.

作者信息

Du Mengmeng, Li Jiajia, Wang Rong, Wu Ying

机构信息

State Key Laboratory for Strength and Vibration of Mechanical Structures, School of Aerospace, Xi'an Jiaotong University, Xi'an, China.

出版信息

Cogn Neurodyn. 2016 Oct;10(5):405-14. doi: 10.1007/s11571-016-9390-4. Epub 2016 May 27.

Abstract

Experiments on hippocampal slices have recorded that a novel pattern of epileptic seizures with alternating excitatory and inhibitory activities in the CA1 region can be induced by an elevated potassium ion (K(+)) concentration in the extracellular space between neurons and astrocytes (ECS-NA). To explore the intrinsic effects of the factors (such as glial K(+) uptake, Na(+)-K(+)-ATPase, the K(+) concentration of the bath solution, and K(+) lateral diffusion) influencing K(+) concentration in the ECS-NA on the epileptic seizures recorded in previous experiments, we present a coupled model composed of excitatory and inhibitory neurons and glia in the CA1 region. Bifurcation diagrams showing the glial K(+) uptake strength with either the Na(+)-K(+)-ATPase pump strength or the bath solution K(+) concentration are obtained for neural epileptic seizures. The K(+) lateral diffusion leads to epileptic seizure in neurons only when the synaptic conductance values of the excitatory and inhibitory neurons are within an appropriate range. Finally, we propose an energy factor to measure the metabolic demand during neuron firing, and the results show that different energy demands for the normal discharges and the pathological epileptic seizures of the coupled neurons.

摘要

对海马切片进行的实验记录表明,通过提高神经元与星形胶质细胞之间细胞外空间(ECS-NA)中的钾离子(K⁺)浓度,可诱导出一种在CA1区域具有兴奋性和抑制性活动交替的新型癫痫发作模式。为了探究影响ECS-NA中K⁺浓度的因素(如胶质细胞对K⁺的摄取、钠钾ATP酶、浴液中的K⁺浓度以及K⁺的横向扩散)对先前实验中记录的癫痫发作的内在影响,我们提出了一个由CA1区域的兴奋性和抑制性神经元以及胶质细胞组成的耦合模型。针对神经性癫痫发作,获得了显示胶质细胞K⁺摄取强度与钠钾ATP酶泵强度或浴液K⁺浓度关系的分岔图。仅当兴奋性和抑制性神经元的突触电导值处于适当范围内时,K⁺的横向扩散才会导致神经元癫痫发作。最后,我们提出了一个能量因子来衡量神经元放电期间的代谢需求,结果表明耦合神经元的正常放电和病理性癫痫发作具有不同的能量需求。

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