title: Role of glial K(+) channels in ontogeny and gliosis: a hypothesis based upon studies on Müller cells.
abstract: The electrophysiological properties of Müller cells, the principal glial cells of the retina, are determined by several types of K(+) conductances. Both the absolute and the relative activities of the individual types of K(+) channels undergo important changes in the course of ontogenetic development and during gliosis. Although immature Müller cells express inwardly rectifying K(+) (K(IR)) currents at a very low density, the membrane of normal mature Müller cells is predominated by the K(IR) conductance. The K(IR) channels mediate spatial buffering K(+) currents and maintain a stable hyperpolarized membrane potential necessary for various glial-neuronal interactions. During "conservative" (i.e., non-proliferative) reactive gliosis, the K(IR) conductance of Müller cells is moderately reduced and the cell membrane is slightly depolarized; however, when gliotic Müller cells become proliferative, their K(IR) conductances are dramatically down-regulated; this is accompanied by an increased activity of Ca(2+)-activated K(+) channels and by a conspicuous unstability of their membrane potential. The resultant variations of the membrane potential may increase the activity of depolarization-activated K(+), Na(+) and Ca(2+) channels. It is concluded that in respect to their K(+) current pattern, mature Müller cells pass through a process of dedifferentiation before proliferative activity is initiated.
authors.affiliation: Department of Neurophysiology, Paul Flechsig Institute of Brain Research, University of Leipzig, Leipzig, Germany. bria@server3.medizin.uni-leipzig.de
authors.forename: A
authors.initials: A
authors.lastname: Bringmann
authors.forename: M
authors.initials: M
authors.lastname: Francke
authors.forename: T
authors.initials: T
authors.lastname: Pannicke
authors.forename: B
authors.initials: B
authors.lastname: Biedermann
authors.forename: H
authors.initials: H
authors.lastname: Kodal
authors.forename: F
authors.initials: F
authors.lastname: Faude
authors.forename: W
authors.initials: W
authors.lastname: Reichelt
authors.forename: A
authors.initials: A
authors.lastname: Reichenbach
mesh_terms: D000818:Animals; D002454:Cell Differentiation / Q000502:physiology; D002455:Cell Division / Q000502:physiology; D005911:Gliosis / Q000378:metabolism / Q000503:physiopathology*; D006801:Humans; D051036:Large-Conductance Calcium-Activated Potassium Channels; D008564:Membrane Potentials / Q000502:physiology; D009457:Neuroglia / Q000378:metabolism*; D011188:Potassium / Q000378:metabolism; D015221:Potassium Channels / Q000378:metabolism / Q000502:physiology*; D024681:Potassium Channels, Calcium-Activated; D024661:Potassium Channels, Inwardly Rectifying; D012160:Retina / Q000166:cytology / Q000378:metabolism* / Q000502:physiology
chemical_list: D051036:Large-Conductance Calcium-Activated Potassium Channels; D015221:Potassium Channels; D024681:Potassium Channels, Calcium-Activated; D024661:Potassium Channels, Inwardly Rectifying; D011188:Potassium