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Effect of Adenosine and Adenosine Receptor Antagonists on Retinal Müller Cell Inwardly Rectifying Potassium Channels under Exogenous Glutamate Stimulation

机译:腺苷和腺苷受体拮抗剂对外源谷氨酸刺激下视网膜Müller细胞内向钾通道的影响

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摘要

The vitreousness of glaucoma subjects contains elevated glutamate, and excessive extracellular glutamate is toxic to retinal neurons. Therefore, glutamate clearance is potentially impaired in the retina of glaucoma subjects. Müller cells play an important role in maintaining low extracellular levels of neurotransmitters, such as glutamate. A better understanding of the cross-talk between adenosine and glutamate may provide a better characterization of the regulatory network in Müller cells. Here, Müller cells were purified from the rat retina on postnatal day 5 using the papain digestion method. Application of increasing concentrations of glutamate (0-20 mmol/L) caused a dose-dependent decrease in the expression levels of Kir4.1, Kir2.1, GLAST, and GS. Exogenous adenosine regulated Kir channels and subsequently promoted GLAST and GS expression levels in Müller cells under exogenous glutamate stimulation. These effects were partly dependent on adenosine receptors.
机译:青光眼受试者的玻璃体含有高水平的谷氨酸盐,过量的细胞外谷氨酸盐对视网膜神经元有毒性。因此,在青光眼受试者的视网膜中谷氨酸盐清除可能受到损害。 Müller细胞在维持低水平的神经递质(如谷氨酸)的细胞外水平中起重要作用。更好地了解腺苷和谷氨酸之间的串扰可以更好地表征Müller细胞中的调节网络。在这里,使用木瓜蛋白酶消化方法在出生后第5天从大鼠视网膜中纯化Müller细胞。逐渐增加浓度的谷氨酸(0-20Lmmol / L)的使用导致Kir4.1,Kir2.1,GLAST和GS的表达水平呈剂量依赖性降低。外源腺苷调节Kir通道,并随后在外源谷氨酸刺激下促进Müller细胞中GLAST和GS表达水平。这些作用部分取决于腺苷受体。

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