Glial and nerve cell changes in rats with porto-caval anastomosis

Nuclear size and density were determined in brain regions with different glial--neurone composition in rats up to 35 weeks after porto-caval anastomosis. In the white matter, i.e. corpus callosum, both the total cell count and the percentage of astrocytes and oligodendrocytes were unchanged. In the...

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Veröffentlicht in:Acta neuropathologica 1977-07, Vol.39 (1), p.59-68
Hauptverfasser: Diemer, N H, Klee, J, Schröder, H, Klinken, L
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Sprache:eng
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Zusammenfassung:Nuclear size and density were determined in brain regions with different glial--neurone composition in rats up to 35 weeks after porto-caval anastomosis. In the white matter, i.e. corpus callosum, both the total cell count and the percentage of astrocytes and oligodendrocytes were unchanged. In the corpus striatum, where the glial/neurone ratio is about 1, the number of nuclei registered as astrocytes increased, and after 35 weeks astrocytes comprised 29% of glial cells (compared with 15% in controls). However, the number of oligodendrogial nuclei decreased simultaneously, leaving the total glial number unchanged. In the animals with longest experimental period there was a 15% loss of neurones. In a region with higher glial/neurone ratio, i.e. the Purkinje cell layer, the neurones showed a similar reduction, whereas the number of Bergmann astrocyte nuclei increased less than striatal astrocytes. A small group of animals with pronounced signs of encephalopathy had a higher loss of neurones and, furthermore, the glial number in corpus striatum and callosum was reduced, due to loss of oligodendrocytes. Despite the use of perfusion fixation, the size of astrocyte nuclei increased, this was reversible, as only slight changes were seen after 35 weeks. A possible explanation of the increase in astrocyte nuclear count and decrease in oligodendroglial count could be that nuclei normally considered to be oligodendroglial are transformed into nuclei with morphological characteristics of astrocytes.
ISSN:0001-6322
1432-0533
DOI:10.1007/BF00690386