Abstract
Ocular inflammation is a common cause of retinal edema that may involve swelling of Müller glial cells. In order to investigate whether endotoxin-induced ocular inflammation in rats alters the swelling and membrane characteristics of Müller cells, lipopolysaccharide (LPS; 0.5%) was intravitreally injected. At 3 and 7 days after treatment, hypotonic challenge induced swelling of Müller cell somata that was not observed in non-treated control eyes. Müller cells of LPS-treated eyes displayed a downregulation of inward K(+) currents and upregulation of A-type K(+) currents that was associated with a decreased expression of Kir4.1 protein in retinal slices. The data suggest that ocular inflammation induces alterations of both the swelling characteristics and the K(+) channel expression of Müller cells.
Publication types
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Comparative Study
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Research Support, Non-U.S. Gov't
MeSH terms
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Analysis of Variance
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Animals
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Cell Size / drug effects
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Cells, Cultured
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Disease Models, Animal
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Dose-Response Relationship, Drug
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Edema / chemically induced
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Edema / pathology
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Edema / physiopathology
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Electric Capacitance
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Electric Stimulation
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Excitatory Amino Acids / pharmacology
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Eye Diseases / chemically induced
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Eye Diseases / pathology*
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Eye Diseases / physiopathology*
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Glial Fibrillary Acidic Protein / metabolism
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Glutamic Acid / pharmacology
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Immunohistochemistry / methods
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Lipopolysaccharides
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Membrane Potentials / physiology*
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Membrane Potentials / radiation effects
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Neuroglia / pathology*
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Patch-Clamp Techniques / methods
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Potassium Channels, Inwardly Rectifying / drug effects
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Potassium Channels, Inwardly Rectifying / metabolism
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Potassium Channels, Inwardly Rectifying / physiology
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Potassium Chloride / pharmacology
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Rats
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Rats, Long-Evans
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Retina / pathology
Substances
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Excitatory Amino Acids
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Glial Fibrillary Acidic Protein
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Kcnj10 (channel)
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Lipopolysaccharides
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Potassium Channels, Inwardly Rectifying
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Glutamic Acid
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Potassium Chloride