Hypoosmotic and glutamate‐induced swelling of bipolar cells in the rat retina: comparison with swelling of Müller glial cells
Hypoosmotic and glutamate‐induced swelling of bipolar cells in the rat retina: comparison with swelling of Müller glial cells
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低渗和谷氨酸诱导的大鼠视网膜双极细胞肿胀：与穆勒胶质细胞肿胀的比较
DOI：
10.1111/jnc.12307
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发表时间：
2013
影响因子：
4.7
通讯作者：
Bringmann A
中科院分区：
文献类型：
--
作者：
Vogler S;Grosche A;Pannicke T;Ulbricht E;Wiedemann P;Reichenbach A;Bringmann A
细胞体积的调节对于避免由细胞外空间体积的减少引起的神经元兴奋性的变化非常重要。我们比较了低渗和谷氨酸刺激条件下视网膜神经胶质（Müller）和神经元（双极）细胞的体积调节。用低渗溶液（60%渗透压; 4 min）或含谷氨酸盐（1 mM）的等渗溶液（15 min）灌注新鲜分离的大鼠视网膜切片，记录Müller和双极细胞胞体的大小变化。双极细胞胞体，但不是米勒细胞胞体，肿胀低渗条件下，在谷氨酸的存在下。双极细胞胞体的低渗肿胀可能是由钠流入细胞介导的，因为在细胞外无钠条件下未观察到，并且是由代谢型谷氨酸受体和钠依赖性谷氨酸转运蛋白的激活诱导的。谷氨酸诱导的双极细胞胞体肿胀由NMDA和非NMDA谷氨酸受体、谷氨酸转运蛋白和电压门控钠通道激活诱导的氯化钠流入细胞介导。谷氨酸诱导的双极细胞胞体肿胀被腺苷和γ-氨基丁酸消除，但不被血管内皮生长因子和ATP消除。这些数据可能表明，Müller细胞，与双极细胞，具有内源性机制，严格调节细胞体积的低渗透压和长期的谷氨酸暴露。抑制性视网膜传递可能通过抑制谷氨酸的兴奋作用来调节双极细胞的体积。
Regulation of cellular volume is of great importance to avoid changes in neuronal excitability resulting from a decrease in the extracellular space volume. We compared the volume regulation of retinal glial (Müller) and neuronal (bipolar) cells under hypoosmotic and glutamate‐stimulated conditions. Freshly isolated slices of the rat retina were superfused with a hypoosmotic solution (60% osmolarity; 4 min) or with a glutamate (1 mM)‐containing isoosmotic solution (15 min), and the size changes of Müller and bipolar cell somata were recorded. Bipolar cell somata, but not Müller cell somata, swelled under hypoosmotic conditions and in the presence of glutamate. The hypoosmotic swelling of bipolar cell somata might be mediated by sodium flux into the cells, because it was not observed under extracellular sodium‐free conditions, and was induced by activation of metabotropic glutamate receptors and sodium‐dependent glutamate transporters. The glutamate‐induced swelling of bipolar cell somata was mediated by sodium chloride flux into the cells induced by activation of NMDA‐ and non‐NMDA glutamate receptors, glutamate transporters, and voltage‐gated sodium channels. The glutamate‐induced swelling of bipolar cell somata was abrogated by adenosine and γ‐aminobutyric acid, but not by vascular endothelial growth factor and ATP. The data may suggest that Müller cells, in contrast to bipolar cells, possess endogenous mechanisms which tightly regulate the cellular volume in response to hypoosmolarity and prolonged glutamate exposure. Inhibitory retinal transmission may regulate the volume of bipolar cells, likely by inhibition of the excitatory action of glutamate.
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