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

机译:钾浓度对海马耦合神经元模型癫痫发作的影响

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摘要

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.
机译:在海马切片上进行的实验表明,神经元与神经元之间的细胞外空间钾离子浓度升高会诱发CA1区具有交替的兴奋性和抑制性活动的癫痫性发作的新模式。星形胶质细胞(ECS-NA)。探讨因素的内在作用(例如神经胶质K + 摄取,Na + –K + -ATPase,K 浴液中的+ 浓度和K + 横向扩散)影响ECS-NA中先前实验记录的癫痫发作的K + 浓度,我们提出了由CA1区域的兴奋性和抑制性神经元和神经胶质组成的耦合模型。分叉图显示神经胶质K + 的吸收强度与Na + –K + -ATPase泵浦强度或浴液K 获得神经癫痫发作的+浓度。仅当兴奋性和抑制性神经元的突触电导值在适当范围内时,K + 的侧向扩散才导致神经元癫痫性发作。最后,我们提出了一种能量因子来测量神经元放电过程中的代谢需求,结果表明耦合神经元的正常放电和病理性癫痫发作的能量需求不同。

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