title: Atypical gliosis in Müller cells of the slowly degenerating rds mutant mouse retina.
abstract: Retinal Müller glial cells are known to undergo reactive changes (gliosis) in various retinal diseases. In virtually all cases studied, an upregulation of glial fibrillary acidic protein (GFAP) and a hypertrophy can be observed. Physiological alterations, such as a strong downregulation of inwardly rectifying K+ (Kir) currents, were found after retinal detachment (man, rabbit) and after ischemia/reperfusion (rat) but not in more slowly progressing retinal degenerations (Borna Disease Virus-infected rats, RCS rats). This led us to hypothesize that Müller cells respond with 'typical' reactive gliosis only to rapid but not to slow retinal degeneration. To test this hypothesis, we studied Müller cells from rds mutant mice (PrphRd2), which show a retinal degeneration of early onset and slow progression, resulting in a complete loss of photoreceptors after 9-12 months. In Müller cells of rds mice, we found immunoreactivity for GFAP, a marker of gliosis in Müller cells, from postnatal day 21 on, accompanied by a moderately increased membrane capacitance (taken as an indicator of hypertrophy), whereas no change in the expression of the Kir4.1 protein occurred in adult rds mice. We failed to observe significant changes in the membrane resistance and the membrane potential of cells from rds mice from first week after birth until 1 year of age. Current densities were decreased in cells from 3- and 5-week old rds mice. Furthermore, as in control cells from wildtype animals, these cells displayed dominant Kir currents, voltage-dependent Na+ currents, and glutamate uptake currents. These data support the idea that in mice as well as previously shown in rats, slow retinal degeneration induces an atypical gliosis of Müller cells.
authors.affiliation: Paul-Flechsig-Institut für Hirnforschung, Universität Leipzig, Jahnallee 59, D-04109 Leipzig, Germany. ianors.iandiev@medizin.uni-leipzig.de
authors.forename: Ianors
authors.initials: I
authors.lastname: Iandiev
authors.forename: Bernd
authors.initials: B
authors.lastname: Biedermann
authors.forename: Andreas
authors.initials: A
authors.lastname: Bringmann
authors.forename: Martin B
authors.initials: MB
authors.lastname: Reichel
authors.forename: Andreas
authors.initials: A
authors.lastname: Reichenbach
authors.forename: Thomas
authors.initials: T
authors.lastname: Pannicke
mesh_terms: D000818:Animals; D015415:Biomarkers / Q000032:analysis; D004594:Electrophysiology; D005904:Glial Fibrillary Acidic Protein / Q000032:analysis; D005911:Gliosis / Q000473:pathology*; D018698:Glutamic Acid / Q000494:pharmacology; D007150:Immunohistochemistry / Q000379:methods; D051379:Mice; D008807:Mice, Inbred BALB C; D008817:Mice, Mutant Strains; D018408:Patch-Clamp Techniques; D015221:Potassium Channels / Q000502:physiology; D024661:Potassium Channels, Inwardly Rectifying / Q000032:analysis; D012160:Retina / Q000378:metabolism / Q000473:pathology*; D012162:Retinal Degeneration / Q000378:metabolism / Q000473:pathology*; D015222:Sodium Channels / Q000502:physiology; D013997:Time Factors; D000098854:Kcnj10 Channel
chemical_list: D015415:Biomarkers; D005904:Glial Fibrillary Acidic Protein; D000098854:Kcnj10 Channel; D015221:Potassium Channels; D024661:Potassium Channels, Inwardly Rectifying; D015222:Sodium Channels; D018698:Glutamic Acid