Source:http://linkedlifedata.com/resource/pubmed/id/10594921
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
1
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pubmed:dateCreated |
2000-1-18
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pubmed:abstractText |
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.
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pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Large-Conductance...,
http://linkedlifedata.com/resource/pubmed/chemical/Potassium,
http://linkedlifedata.com/resource/pubmed/chemical/Potassium Channels,
http://linkedlifedata.com/resource/pubmed/chemical/Potassium Channels...,
http://linkedlifedata.com/resource/pubmed/chemical/Potassium Channels, Inwardly...
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pubmed:status |
MEDLINE
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pubmed:month |
Jan
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pubmed:issn |
0894-1491
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pubmed:author | |
pubmed:copyrightInfo |
Copyright 2000 Wiley-Liss, Inc.
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pubmed:issnType |
Print
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pubmed:day |
1
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pubmed:volume |
29
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
35-44
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pubmed:dateRevised |
2006-11-15
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pubmed:meshHeading |
pubmed-meshheading:10594921-Animals,
pubmed-meshheading:10594921-Cell Differentiation,
pubmed-meshheading:10594921-Cell Division,
pubmed-meshheading:10594921-Gliosis,
pubmed-meshheading:10594921-Humans,
pubmed-meshheading:10594921-Large-Conductance Calcium-Activated Potassium Channels,
pubmed-meshheading:10594921-Membrane Potentials,
pubmed-meshheading:10594921-Neuroglia,
pubmed-meshheading:10594921-Potassium,
pubmed-meshheading:10594921-Potassium Channels,
pubmed-meshheading:10594921-Potassium Channels, Calcium-Activated,
pubmed-meshheading:10594921-Potassium Channels, Inwardly Rectifying,
pubmed-meshheading:10594921-Retina
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pubmed:year |
2000
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pubmed:articleTitle |
Role of glial K(+) channels in ontogeny and gliosis: a hypothesis based upon studies on Müller cells.
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pubmed:affiliation |
Department of Neurophysiology, Paul Flechsig Institute of Brain Research, University of Leipzig, Leipzig, Germany. bria@server3.medizin.uni-leipzig.de
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pubmed:publicationType |
Journal Article,
Review,
Research Support, Non-U.S. Gov't
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