Analysis of potassium ion diffusion from neurons to capillaries: Effects of astrocyte endfeet geometry.

Analysis of potassium ion diffusion from neurons to capillaries: Effects of astrocyte endfeet geometry.
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钾离子从神经元到毛细血管的扩散分析:星形胶质细胞末端几何形状的影响。

DOI:
10.1111/ejn.16232
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发表时间:
2024
期刊:
The European journal of neuroscience
影响因子:
--
通讯作者:
Secomb,TimothyW
Secomb,TimothyW
中科院分区:
--
文献类型:
--
作者:
Djurich,Sara;Secomb,TimothyW

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神经血管偶联(NVC)是指脑血流量的局部增加,以响应增加的神经元活动。神经元和血管之间的通讯机制仍不清楚。星形胶质细胞终足几乎完全覆盖脑毛细血管,表明星形胶质细胞通过在毛细血管附近释放血管活性物质在NVC中发挥作用。另一种假设是,神经元释放的钾离子(K+)通过细胞外间隙的直接扩散有助于NVC。在这里,目标是确定星形胶质细胞终足是否存在K+从神经元扩散到毛细血管的障碍。使用了两种简化的细胞外空间、端足之间的裂缝和血管周围空间的2D几何形状:(i)距离毛细血管1 μm的源;(ii)距离毛细血管15 μm的神经元。K+释放被建模为细胞外间隙外边界处[K+]的阶跃增加。数值求解时间相关扩散方程。在第一种几何结构中,血管周围[K+]在0.05 s内接近其最终值。减小足端裂宽度或增加血管周围间隙宽度可减缓[K+]的升高。在第二种几何形状中,血管周围[K+]的增加发生在0.5 s内,并且对裂隙宽度或血管周围空间宽度的变化不敏感。血管周围[K+]的预测水平足以引起血管舒张,并且上升时间在NVC中流量增加的时间内。这些结果表明,直接扩散的K+通过细胞外空间是一个可能的NVC信号机制。
Neurovascular coupling (NVC) refers to a local increase in cerebral blood flow in response to increased neuronal activity. Mechanisms of communication between neurons and blood vessels remain unclear. Astrocyte endfeet almost completely cover cerebral capillaries, suggesting that astrocytes play a role in NVC by releasing vasoactive substances near capillaries. An alternative hypothesis is that direct diffusion through the extracellular space of potassium ions (K+) released by neurons contributes to NVC. Here, the goal is to determine whether astrocyte endfeet present a barrier to K+diffusion from neurons to capillaries. Two simplified 2D geometries of extracellular space, clefts between endfeet, and perivascular space are used: (i) a source 1 μm from a capillary; (ii) a neuron 15 μm from a capillary. K+release is modelled as a step increase in [K+] at the outer boundary of the extracellular space. The time‐dependent diffusion equation is solved numerically. In the first geometry, perivascular [K+] approaches its final value within 0.05 s. Decreasing endfeet cleft width or increasing perivascular space width slows the rise in [K+]. In the second geometry, the increase in perivascular [K+] occurs within 0.5 s and is insensitive to changes in cleft width or perivascular space width. Predicted levels of perivascular [K+] are sufficient to cause vasodilation, and the rise time is within the time for flow increase in NVC. These results suggest that direct diffusion of K+through the extracellular space is a possible NVC signalling mechanism.
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