Paul-Flechsig-Institut für Hirnforschung, Universität Leipzig, Jahnallee 59, D-04109 Leipzig, Germany.
Neurosci Lett. 2010 Mar 12;472(1):73-8. doi: 10.1016/j.neulet.2010.01.062. Epub 2010 Feb 2.
Retinal Müller glial cells are involved in K+ ion homeostasis of the tissue. Inwardly rectifying K(+) (Kir) channels play a decisive role in the process of spatial K+ buffering. It has been demonstrated that Kir-mediated currents of Müller cells are downregulated in various cases of retinal neurodegeneration. However, this has not yet been verified for any murine animal model. The aim of the present study was to investigate Müller cells after transient retinal ischemia in mice. High intraocular pressure was applied for 1h; the retina was analysed 1 week later. We studied protein expression in the tissue by immunohistochemistry, and membrane currents of isolated cells by patch-clamp experiments. We found the typical indicators of reactive gliosis such as upregulation of glial fibrillary acidic protein. Moreover, the membrane capacitance of isolated Müller cells was increased and the amplitudes of Kir-mediated currents were slightly, but significantly decreased. This murine high intraocular pressure model of transient retinal ischemia is proposed as a versatile tool for further studies on Müller cell functions in retinal degeneration.
视网膜 Müller 胶质细胞参与组织内 K+ 离子的动态平衡。内向整流钾（Kir）通道在空间 K+缓冲过程中起决定性作用。已经证明，在各种视网膜神经退行性变的情况下，Müller 细胞的 Kir 介导电流受到下调。然而，这尚未在任何小鼠动物模型中得到验证。本研究的目的是在小鼠短暂性视网膜缺血后研究 Müller 细胞。施加 1 小时的高眼压；1 周后分析视网膜。我们通过免疫组织化学研究组织中的蛋白表达，并通过膜片钳实验研究分离细胞的膜电流。我们发现了反应性神经胶质增生的典型标志物，如神经胶质纤维酸性蛋白的上调。此外，分离的 Müller 细胞的膜电容增加，Kir 介导的电流幅度略有但显著降低。这种小鼠短暂性视网膜缺血的高眼压模型被提议作为进一步研究视网膜变性中 Müller 细胞功能的通用工具。
