title: Müller cell gliosis in retinal organ culture mimics gliotic alterations after ischemia in vivo.
abstract: A decrease in the expression of inwardly rectifying potassium (Kir) currents is a characteristic feature of retinal glial (Müller) cells in various retinopathies, e.g., after transient retinal ischemia. We used short-term retinal organ cultures to investigate whether similar physiological alterations can be induced under in vitro conditions. During 4 days in vitro, Müller cells displayed a decrease in Kir currents and an increase in transient A-type potassium currents which was similar to the alterations in membrane physiology during ischemia-reperfusion in vivo. In addition, gliosis of Müller cells both in vivo and in organ cultures was associated with cellular hypertrophy and an alteration in osmotic swelling characteristics. Whereas Müller cells in control retinae did not swell under hypotonic stress, cells in postischemic retinae and in organ cultures swelled upon hypotonic challenge. Therefore, Müller cells in organ cultures can be used to investigate distinct aspects of ischemia-induced Müller cell gliosis. Both the decrease in Kir currents and the alteration in osmotic swelling may reflect a dysfunction of Müller cells regarding the control of the ionic and osmotic homeostasis in the retina.
authors.affiliation: Paul Flechsig Institute of Brain Research, University of Leipzig, Faculty of Medicine, Jahnallee 59, 04109 Leipzig, Germany.
authors.forename: Heidrun
authors.initials: H
authors.lastname: Kuhrt
authors.forename: Antje
authors.initials: A
authors.lastname: Wurm
authors.forename: Anett
authors.initials: A
authors.lastname: Karl
authors.forename: Ianors
authors.initials: I
authors.lastname: Iandiev
authors.forename: Peter
authors.initials: P
authors.lastname: Wiedemann
authors.forename: Andreas
authors.initials: A
authors.lastname: Reichenbach
authors.forename: Andreas
authors.initials: A
authors.lastname: Bringmann
authors.forename: Thomas
authors.initials: T
authors.lastname: Pannicke
mesh_terms: D000818:Animals; D051401:Aquaporin 4 / Q000378:metabolism; D015415:Biomarkers / Q000378:metabolism; D002545:Brain Ischemia / Q000473:pathology / Q000503:physiopathology*; D048429:Cell Size / Q000187:drug effects; D002478:Cells, Cultured; D005904:Glial Fibrillary Acidic Protein / Q000378:metabolism; D005911:Gliosis / Q000473:pathology / Q000503:physiopathology*; D007038:Hypotonic Solutions / Q000494:pharmacology; D008564:Membrane Potentials / Q000187:drug effects / Q000502:physiology; D009457:Neuroglia / Q000187:drug effects / Q000473:pathology / Q000502:physiology*; D009924:Organ Culture Techniques; D024661:Potassium Channels, Inwardly Rectifying / Q000378:metabolism / Q000502:physiology; D051381:Rats; D020318:Rats, Long-Evans; D015427:Reperfusion Injury / Q000473:pathology / Q000503:physiopathology; D012160:Retina / Q000187:drug effects / Q000473:pathology / Q000503:physiopathology; D012164:Retinal Diseases / Q000473:pathology / Q000503:physiopathology*; D014882:Water-Electrolyte Balance / Q000187:drug effects / Q000502:physiology*; D000098854:Kcnj10 Channel
chemical_list: C496032:Aqp4 protein, rat; D051401:Aquaporin 4; D015415:Biomarkers; D005904:Glial Fibrillary Acidic Protein; D007038:Hypotonic Solutions; D000098854:Kcnj10 Channel; D024661:Potassium Channels, Inwardly Rectifying