Reduced Ca2+ flux in synaptosomes from cats with GM1 gangliosidosis

Michael L. Koenig, Richard S. Jope, Henry J. Baker, Kathleen M. Lally

Research output: Contribution to journalArticle

15 Scopus citations

Abstract

Ca2+ transport was studied in synaptosomes prepared from normal cats and cats with GM1 gangliosidosis. The influx of Ca2+ was found to be a biphasic process in synaptosomes from both GM1 mutant and normal cats. Both the fast and slow phases of voltage-dependent Ca2+ uptake were significantly reduced in cats with the lysosomal storage disease, however the inhibitory mechanisms differed. The fast phase of Ca2+ uptake was inhibited uncompetitively, whereas the slow phase was inhibited competitively. In addition, Na+-dependent Ca2+ efflux was reduced significantly in cats with GM1 gangliosidosis. Since it is well established that maintenance of Ca2+ homeostatis is essential for normal neuronal function, a ganglioside-induced disruption of Ca2+ transport across synaptic membranes may be responsible, in part, for the neuronal dysfunction characteristic of GM1 gangliosidosis.

Original languageEnglish (US)
Pages (from-to)169-176
Number of pages8
JournalBrain Research
Volume424
Issue number1
DOIs
StatePublished - Oct 20 1987
Externally publishedYes

Keywords

  • Calcium flux
  • G gangliosidosis
  • Synaptosome

ASJC Scopus subject areas

  • Developmental Biology
  • Molecular Biology
  • Clinical Neurology
  • Neuroscience(all)

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