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

Overview

MeSH Major

  • Calcium
  • Homeostasis
  • Motor Neurons
  • Oculomotor Nerve
  • Spinal Cord
  • Superoxide Dismutase

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.

publication date

  • May 2000

Research

keywords

  • Academic Article

Identity

Language

  • eng

PubMed ID

  • 10805095

Additional Document Info

start page

  • 517

end page

  • 24

volume

  • 99

number

  • 5