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首页> 外文期刊>Journal of Computational Neuroscience >Dependence of spontaneous neuronal firing and depolarisation block on astroglial membrane transport mechanisms
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Dependence of spontaneous neuronal firing and depolarisation block on astroglial membrane transport mechanisms

机译：自发性神经元放电和去极化阻滞对星形胶质细胞膜转运机制的依赖性

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摘要

Exposed to a sufficiently high extracellular potassium concentration ([K~+]_o), the neuron can fire spontaneous discharges or even become inactivated due to membrane depolarisation ('depolarisation block'). Since these phenomena likely are related to the maintenance and propagation of seizure discharges, it is of considerable importance to understand the conditions under which excess [K~+]_o causes them. To address the putative effect of glial buffering on neuronal activity under elevated [K~+]_o conditions, we combined a recently developed dynamical model of glial membrane ion and water transport with a Hodgkin-Huxley type neuron model. In this interconnected glia-neuron model we investigated the effects of natural heterogeneity or pathological changes in glial membrane transporter density by considering a large set of models with different, yet empirically plausible, sets of model parameters. We observed both the high [K~+]_o-induced duration of spontaneous neuronal firing and the prevalence of depolarisation block to increase when reducing the magnitudes of the glial transport mechanisms. Further, in some parameter regions an oscillatory bursting spiking pattern due to the dynamical coupling of neurons and glia was observed. Bifurcation analyses of the neuron model and of a simplified version of the neuron-glia model revealed further insights about the underlying mechanism behind these phenomena. The above insights emphasise the importance of combining neuron models with detailed astroglial models when addressing phenomena suspected to be influenced by the astroglia-neuron interaction. To facilitate the use of our neuron-glia model, a CellML version of it is made publicly available.
机译：暴露于足够高的细胞外钾浓度（[K〜+] _ o）时，神经元会自发放电，甚至由于膜去极化（“去极化阻滞”）而失活。由于这些现象可能与癫痫发作放电的维持和传播有关，因此了解过量[K〜+] _ o引起癫痫发作的条件非常重要。为了解决在升高的[K〜+] _ o条件下神经胶质缓冲作用对神经元活动的推定作用，我们将最近开发的神经胶质膜离子和水运输动力学模型与霍奇金-赫克斯利型神经元模型相结合。在此互连的神经胶质-神经元模型中，我们通过考虑大量具有不同但经验上合理的模型参数的模型，研究了自然异质性或胶质膜转运蛋白密度病理变化的影响。我们观察到高[K〜+] _ o诱导的自发神经元放电持续时间和去极化阻滞的发生率在降低神经胶质运输机制的强度时均会增加。此外，在某些参数区域中，观察到由于神经元和神经胶质的动态耦合而产生的振荡性突刺模式。神经元模型和神经元神经胶质模型的简化版本的分叉分析揭示了关于这些现象背后的潜在机制的进一步见解。上述见解强调了在解决怀疑受星形胶质-神经元相互作用影响的现象时，将神经元模型与详细的星形胶质模型相结合的重要性。为了方便使用我们的神经胶质细胞模型，其CellML版本已公开提供。

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  • 来源
    《Journal of Computational Neuroscience》 |2012年第1期|p.147-165|共19页
  • 作者

    Leiv Oyehaug; Ivar Ostby; Catherine M. Lloyd; Stig W. Omholt; Gaute T. Einevoll;

  • 作者单位

    Centre for Integrative Genetics (CIGENE),Department of Mathematical Sciences and Technology,Norwegian University of Life Sciences, 1430 As, Norway,Institute for Experimental Medical Research,and Center for Heart Failure Research,University of Oslo, Oslo, Norway;

    Centre for Integrative Genetics (CIGENE),Department of Mathematical Sciences and Technology,Norwegian University of Life Sciences, 1430 As, Norway;

    Auckland Bioengineering Institute,The University of Auckland, Auckland, New Zealand;

    Centre for Integrative Genetics (CIGENE),Department of Animal and Aquacultural Sciences,Norwegian University of Life Sciences, 1430 As, Norway;

    Centre for Integrative Genetics (CIGENE),Department of Mathematical Sciences and Technology,Norwegian University of Life Sciences, 1430 As, Norway;

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  • 正文语种 eng
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  • 关键词

    potassium dynamics; positive feedback; spontaneous discharges; depolarisation block; glia;

    机译：钾动力学正面反馈;自发放电去极化块;胶质细胞;

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