Retinal glial (Müller) cells are proposed to mediate
retinal potassium homeostasis predominantly by
potassium transport through inwardly rectifying K(+) (Kir) channels.
Retinal gliosis is often associated with a decrease in glial
potassium conductance. To determine whether this decrease is caused by a downregulation of glial Kir channels, we investigated a rabbit model of
proliferative vitreoretinopathy (PVR) which is known to be associated with proliferative
gliosis. The membrane conductance of control Müller cells is characterized by large Kir currents whereas Müller cells of PVR retinas displayed an almost total absence of Kir currents. In control tissues, Kir2.1 immunoreactivity is localized in the inner stem processes and endfeet of Müller cells whereas Kir4.1 immunoreactivity is largely confined to the Müller cell endfeet. In PVR retinas, there is a mislocation of Kir channel
proteins, with Kir4.1 immunoreactivity detectable in Müller cell fibers throughout the whole retina, and a decrease of immunoreactivity in the cellular endfeet. Real-time PCR analysis revealed no alteration of the Kir4.1
mRNA levels in PVR retinas as compared to the controls but a slight decrease in Kir2.1
mRNA. Western blotting showed no difference in the
Kir4.1 protein content between control and PVR retinas. The data suggest that proliferative
gliosis in the retina is associated with a functional inactivation of glial Kir channels that is not caused by a downregulation of the channel
proteins but is associated with their mislocation in the cell membrane.