Cerebellar ganglioside abnormalities in pcd mutant mice

T. N. Seyfried, Robert K Yu

Research output: Contribution to journalArticle

13 Citations (Scopus)

Abstract

The distribution of cerebellar gangliosides was studied in Purkinje cell degeneration pcd/pcd mutant mice at postnatal days 25, 30, 50, and 150. These mutants lose the majority of Purkinje cells between 18 and 50 days of age. A reactive gliosis accompanies Purkinje cell loss and a partial loss of granule cells occurs in pcd/pcd mice older than p50. Purkinje cell loss is associated with significant reductions in cerebellar weight and ganglioside concentration. This neuronal loss was also developmentally correlated with reductions of gangliosides GT1a/LD1 and GT1b and with elevations of GD3. These results agree with previous findings in other cerebellar mutants that GT1a/LD1 and GT1b are concentrated in Purkinje cells and that GD3 is enriched in reactive glial cells. A slight, but significant, reduction in GD1a concentration occurred only in older pcd/pcd mice, consistent with previous findings in weaver and staggerer mice that GD1a is enriched in mature granule cells. The findings with pcd/pcd and other neurological mutants indicate that certain gangliosides can serve as cell‐surface markers for monitoring changes in cerebellar cytoarchitecture that accompany development or disease.

Original languageEnglish (US)
Pages (from-to)105-111
Number of pages7
JournalJournal of Neuroscience Research
Volume26
Issue number1
DOIs
StatePublished - Jan 1 1990
Externally publishedYes

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Gangliosides
Purkinje Cells
Neurologic Mutant Mice
Gliosis
Neuroglia
Weights and Measures

Keywords

  • Purkinje cells
  • cerebellum
  • gangliosides
  • mouse mutants
  • reactive gliosis

ASJC Scopus subject areas

  • Cellular and Molecular Neuroscience

Cite this

Cerebellar ganglioside abnormalities in pcd mutant mice. / Seyfried, T. N.; Yu, Robert K.

In: Journal of Neuroscience Research, Vol. 26, No. 1, 01.01.1990, p. 105-111.

Research output: Contribution to journalArticle

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