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  Use of primary cultures and continuous cell lines to study effects on astrocytic regulatory functions

Walum, E., Eriksson, G., Peterson, A., Holme, E., Larsson, N., Eriksson, C., et al. (1995). Use of primary cultures and continuous cell lines to study effects on astrocytic regulatory functions. Clin Exp Pharmacol Physiol, 22(4), 284-7.

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 Urheber:
Walum, E., Autor
Eriksson, G., Autor
Peterson, A., Autor
Holme, E., Autor
Larsson, N.G.1, Autor           
Eriksson, C., Autor
el-Shamy, W., Autor
Affiliations:
1Department Larsson - Mitochondrial Biology, Max Planck Institute for Biology of Ageing, Max Planck Society, ou_1942286              

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Schlagwörter: Amyotrophic Lateral Sclerosis/metabolism/pathology Animals Astrocytes/*cytology/drug effects/physiology Biological Transport, Active Cell Line Cells, Cultured Energy Metabolism Glutamic Acid/*metabolism Metals/toxicity Oxygen Consumption/physiology Rats Solvents/toxicity
 Zusammenfassung: 1. Current opinions on the mechanisms for glutamate-mediated neurotoxicity are reviewed. The protective role of astrocytic high-affinity glutamate transport is also discussed. 2. Low-density seeding of primary astrocytes from rat hemispheres was found to result in the development of reactive-like astrocytes. Typical glial signs of amyotrophic lateral sclerosis (ALS) could not be induced in astrocyte cultures by serum from ALS-patients. 3. Glutamate (100 mumol/L) was found to induce an increase in respiratory activity in primary cultures of astrocytes. This stimulation appeared to be related to the co-transport of Na2+ with glutamate and a resulting activation of Na2+/K(+)-ATPase. Both basal respiration and glutamate-stimulated oxygen consumption was inhibited by organic solvents. 4. Preliminary results show that heavy metals cause an increase in the mitochondrial DNA content at concentrations that have no effect on growth rate or morphology in a glial cell line. This increase was accompanied by an inhibition of oxygen consumption and an increased production of lactate at unaltered ATP levels.

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 Datum: 1995-041995-04-01
 Publikationsstatus: Erschienen
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 Art der Begutachtung: -
 Identifikatoren: Anderer: 7671442
ISSN: 0305-1870 (Print)0305-1870
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Titel: Clin Exp Pharmacol Physiol
  Alternativer Titel : Clinical and experimental pharmacology & physiology
Genre der Quelle: Zeitschrift
 Urheber:
Affiliations:
Ort, Verlag, Ausgabe: -
Seiten: - Band / Heft: 22 (4) Artikelnummer: - Start- / Endseite: 284 - 7 Identifikator: -