title: Glial cell-mediated spread of retinal degeneration during detachment: a hypothesis based upon studies in rabbits.
abstract: In human subjects with peripheral retinal detachments, visual deficits are not restricted to the detached retina but are also present in the non-detached tissue. Based upon studies on a rabbit model of rhegmatogenous retinal detachment, we propose a glial cell-mediated mechanism of spread of retinal degeneration into non-detached retinal areas which may also have importance for the understanding of alterations in the human retina. Both detached and attached portions of the rabbit retina display photoreceptor cell degeneration and cystic degeneration of the innermost layers. An inverse mode of photoreceptor cell degeneration in the attached tissue suggests a disturbed support of the photoreceptor cells by Müller cells which show various indications of gliosis (increased expression of intermediate filaments, cell hypertrophy, decreased plasma membrane K(+) conductance, increased Ca(2+) responsiveness to purinergic stimulation) in both detached and attached tissues. We propose that gliotic alterations of Müller cells contribute to the degeneration of the attached retina, via disturbance of glial homeostasis mechanisms. A down-regulation of the K(+) conductance of Müller cells may prevent effective retinal K(+) and water clearance, and may favor photoreceptor cell degeneration and edema development.
authors.affiliation: Paul Flechsig Institute of Brain Research, University of Leipzig, D-04109 Leipzig, Germany.
authors.forename: Mike
authors.initials: M
authors.lastname: Francke
authors.forename: Frank
authors.initials: F
authors.lastname: Faude
authors.forename: Thomas
authors.initials: T
authors.lastname: Pannicke
authors.forename: Ortrud
authors.initials: O
authors.lastname: Uckermann
authors.forename: Michael
authors.initials: M
authors.lastname: Weick
authors.forename: Hartwig
authors.initials: H
authors.lastname: Wolburg
authors.forename: Peter
authors.initials: P
authors.lastname: Wiedemann
authors.forename: Andreas
authors.initials: A
authors.lastname: Reichenbach
authors.forename: Susann
authors.initials: S
authors.lastname: Uhlmann
authors.forename: Andreas
authors.initials: A
authors.lastname: Bringmann
mesh_terms: D000255:Adenosine Triphosphate / Q000378:metabolism; D000818:Animals; D002118:Calcium / Q000378:metabolism; D016923:Cell Death / Q000502:physiology; D003560:Cysts / Q000473:pathology; D004487:Edema / Q000473:pathology / Q000503:physiopathology; D005904:Glial Fibrillary Acidic Protein / Q000032:analysis; D006801:Humans; D023421:Models, Animal; D009457:Neuroglia / Q000502:physiology*; D010786:Photoreceptor Cells / Q000473:pathology / Q000503:physiopathology; D011188:Potassium / Q000378:metabolism; D015221:Potassium Channels / Q000378:metabolism; D011817:Rabbits; D018048:Receptors, Purinergic P2 / Q000378:metabolism; D012160:Retina / Q000473:pathology / Q000503:physiopathology; D012162:Retinal Degeneration / Q000473:pathology / Q000503:physiopathology*; D012163:Retinal Detachment / Q000473:pathology / Q000503:physiopathology*; D014786:Vision Disorders / Q000209:etiology / Q000503:physiopathology
chemical_list: D005904:Glial Fibrillary Acidic Protein; D015221:Potassium Channels; D018048:Receptors, Purinergic P2; D000255:Adenosine Triphosphate; D011188:Potassium; D002118:Calcium