Altered calcium homeostasis in spinal motoneurons but not in oculomotor neurons of SOD-1 knockout mice

László Siklós, József I. Engelhardt, Andrew G. Reaume, Richard W. Scott, Róbert Adalbert, Izabella Obál, Stanley H. Appel

Research output: Contribution to journalArticle

15 Citations (Scopus)

Abstract

SOD-1-deficient mice demonstrate no loss of motoneurons but are still vulnerable to axotomy and ischemic insults. To investigate possible reasons for vulnerability of motoneuron populations, we studied changes in ultrastructural calcium distribution during maturation in spinal- and oculomotor neurons in SOD-1(-/-) mice. Between 3 and 11 months the cytoplasmic component of the intracellular calcium changed at a lower rate in spinal motoneurons and motor axon terminals in the interosseus muscle of SOD-1(-/-) animals compared to wild-type controls. No such dissimilarities were noted in the oculomotor system, or in mitochondrial calcium contents of either cell type. These data suggest that the lack of SOD-1 may be associated with vulnerability to insult by depletion of non-mitochondrial calcium stores selectively in motoneurons lacking parvalbumin and/or calbindin D28K.

Original languageEnglish
Pages (from-to)517-524
Number of pages8
JournalActa neuropathologica
Volume99
Issue number5
DOIs
Publication statusPublished - May 2000

Keywords

  • Calcium
  • Knockout mouse
  • Motoneuron
  • Parvalbumin
  • SOD-1

ASJC Scopus subject areas

  • Pathology and Forensic Medicine
  • Clinical Neurology
  • Cellular and Molecular Neuroscience

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