Alterations in protein expression and membrane properties during Muller cell gliosis in a murine model of transient retinal ischemia

作者：Hirrlinger Petra G; Ulbricht Elke; Iandiev Ianors; Reichenbach Andreas; Pannicke Thomas^*

来源：Neuroscience Letters, 2010, 472(1): 73-78.

DOI：10.1016/j.neulet.2010.01.062

• Retina
• Glia
• Ischemia
• K(+) channel

Retinal Muller 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 Muller 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 Muller cells after transient retinal ischemia in mice. High intraocular pressure was applied for 1 h; 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 Killer 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 Muller cell functions in retinal degeneration.

• 出版日期2010-3-12