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      Differential regulation of Kir4.1 and Kir2.1 expression in the ischemic rat retina.

      Neuroscience Letters

      Animals, Cells, Cultured, Gene Expression Regulation, Ischemia, metabolism, Neuroglia, Optic Neuropathy, Ischemic, Potassium Channels, Inwardly Rectifying, Rats, Rats, Long-Evans, Retina, Retinal Vessels, Tissue Distribution

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          Abstract

          Ischemia-reperfusion of the rat retina causes gliosis of Müller cells that is associated with a decrease of their K+ conductance. By using quantitative PCR and immunohistochemical staining of retinal slices, we investigated the effect of transient ischemia-reperfusion on retinal expression of two inward-rectifying K+ (Kir) channels, Kir4.1 and Kir2.1. In control retinas, Müller cells prominently expressed both Kir4.1 and Kir2.1 proteins. At 7 days after reperfusion, the expression of Kir4.1 protein was strongly downregulated, while the Kir2.1 protein expression remained unaltered. The expression of Kir4.1 mRNA was reduced by 55% after ischemia while the expression of Kir2.1 mRNA was not altered. The data suggest that the glial expression of distinct Kir channels is differentially regulated after retinal ischemia, with deletarious consequences for K+ ion and water homeostasis.

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          Journal
          16330144
          10.1016/j.neulet.2005.11.016

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