Linked Life Data

10022343

Source:http://linkedlifedata.com/resource/pubmed/id/10022343

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
1999-5-7
pubmed:abstractText
Retinal explant cultures have been established as a useful tool to study both the normal development of the mammalian retina and the effects of pathogenic agents. We used such cultures as a model for the (ammonia-induced) hepatic retinopathy, earlier observed in humans with chronical liver failure, and ascribed to a breakdown of Müller (glial) cell function. In the explant cultures, one day exposure to elevated (7 mM) ammonia was sufficient to cause Müller cell reactivity as indicated by increasing immunopositivity for glial fibrillary acidic protein. After 4 days in elevated ammonia, the Müller cells were severely deformed, the layered structure of the retinae became disorganized, and significant neuronal cell death occurred. Using whole-cell voltage-clamp recordings, the expression of K+ channels was compared in Müller cells isolated from retinae of rabbits at postnatal days 9 to 12 and from neonatal explants cultured for 9 to 12 days, respectively. Müller glial cells grown both in vivo and in vitro express the same set of K+ channels in their membranes: (i) inwardly rectifying K+ (K(IR)) channels which were selectively blocked by Ba2+ ions; (ii) large-conductance, Ca2+-activated K+ (BK(Ca)) channels which were blocked by iberiotoxin and were activated by phloretin; and (iii) delayed rectifying voltage-gated K+ channels. The presence of K(IR) channels indicates successful differentiation of the Müller cells grown in vitro, as these channels are not expressed in cells from neonatal animals. Four days of elevated ammonia in the culture medium caused a complete loss of K(IR) channels in Müller cell membranes, and a significant decrease of the membrane potential. The results indicate that in hepatic retinopathy, the well-known morphological and enzymatical alterations of Müller glial cells may be accompanied by changes in their membrane permeability for K+.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:issn
0021-8359
pubmed:author
pubmed:issnType
Print
pubmed:volume
39
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
193-206
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed-meshheading:10022343-4-Aminopyridine, pubmed-meshheading:10022343-Ammonia, pubmed-meshheading:10022343-Animals, pubmed-meshheading:10022343-Animals, Newborn, pubmed-meshheading:10022343-Barium, pubmed-meshheading:10022343-Cell Membrane, pubmed-meshheading:10022343-Electrophysiology, pubmed-meshheading:10022343-Glial Fibrillary Acidic Protein, pubmed-meshheading:10022343-Immunohistochemistry, pubmed-meshheading:10022343-Large-Conductance Calcium-Activated Potassium Channels, pubmed-meshheading:10022343-Membrane Potentials, pubmed-meshheading:10022343-Neuroglia, pubmed-meshheading:10022343-Organ Culture Techniques, pubmed-meshheading:10022343-Patch-Clamp Techniques, pubmed-meshheading:10022343-Peptides, pubmed-meshheading:10022343-Potassium Channels, pubmed-meshheading:10022343-Potassium Channels, Calcium-Activated, pubmed-meshheading:10022343-Rabbits, pubmed-meshheading:10022343-Retina, pubmed-meshheading:10022343-Toxins, Biological, pubmed-meshheading:10022343-Vimentin
pubmed:year
1998
pubmed:articleTitle
Müller (glial) cell development in vivo and in retinal explant cultures: morphology and electrophysiology, and the effects of elevated ammonia.
pubmed:affiliation
Paul Flechsig Institute for Brain Research, Department of Neurophysiology, Leipzig University, Germany.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't