Astrocytes form large networks, in which individual cells are connected via gap junctions. It is thought that this astroglial gap junction coupling contributes to the buffering of extracellular K+ increases. However, it is largely unknown how the control of extracellular K+ by astroglial gap junction coupling depends on the underlying activity patterns and on the magnitude of extracellular K+ increases. We explored this dependency in acute hippocampal slices (CA1, stratum radiatum) by direct K+ -sensitive microelectrode recordings and acute pharmacological inhibition of gap junctions. K+ transients evoked by synaptic and axonal activity were largely unaffected by acute astroglial uncoupling in slices obtained from young and adult rats. Iontophoretic K+ -application enabled us to generate K+ gradients with defined spatial properties and magnitude. By varying the K+ -iontophoresis position and protocol, we found that acute pharmacological uncoupling increases the amplitude of K+ transients once their initial amplitude exceeded ~10 mM. Our experiments demonstrate that the contribution of gap junction coupling to buffering of extracellular K+ gradients is limited to large and localized K+ increases.

中文翻译：

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星形胶质间隙连接偶联对CA1层放射状细胞外K +的缓冲作用有限。

星形胶质细胞形成大型网络，其中单个细胞通过间隙连接连接。认为这种星形胶质间隙连接偶联有助于缓冲细胞外K +的增加。然而，很大程度上未知的是，星形胶质间隙连接偶联对细胞外K +的控制如何取决于潜在的活动模式以及细胞外K +的增加幅度。我们通过直接的K +敏感的微电极记录和间隙连接的急性药理学抑制作用探索了在急性海马切片（CA1，放射状层）中的这种依赖性。突触和轴突活动引起的K +瞬变在很大程度上不受幼年和成年大鼠切片中急性星形胶质细胞解偶联的影响。离子电渗的K +应用使我们能够生成具有定义的空间属性和大小的K +梯度。通过改变K +离子电渗疗法的位置和方案，我们发现，一旦其初始幅度超过〜10 mM，急性药理学解偶联会增加K +瞬变的幅度。我们的实验表明，间隙连接偶联对胞外K +梯度缓冲的贡献仅限于较大且局部的K +增加。