Levels of membrane fluidity in the spinal cord and the brain in an animal model of amyotrophic lateral sclerosis

J Bioenerg Biomembr. 2011 Apr;43(2):181-6. doi: 10.1007/s10863-011-9348-5. Epub 2011 Mar 31.


A mutant form of the copper/zinc superoxide dismutase (SOD1) protein is found in some patients with amyotrophic lateral sclerosis (ALS). Alteration of the activity of this antioxidant enzyme leads to an oxidative stress imbalance, which damages the structure of lipids and proteins in the CNS. Using fluorescence spectroscopy, we monitored membrane fluidity in the spinal cord and the brain in a widely used animal model of ALS, the SOD(G93A) mouse, which develops symptoms similar to ALS with an accelerated course. Our results show that the membrane fluidity of the spinal cord in this animal model significantly decreased in symptomatic animals compared with age-matched littermate controls. To the best of our knowledge, this is the first report showing that membrane fluidity is affected in the spinal cord of a SOD(G93A) animal model of ALS. Changes in membrane fluidity likely contribute substantially to alterations in cell membrane functions in the nervous tissue from SOD(G93A) mice.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Amyotrophic Lateral Sclerosis / genetics
  • Amyotrophic Lateral Sclerosis / metabolism*
  • Amyotrophic Lateral Sclerosis / pathology
  • Animals
  • Brain / metabolism*
  • Brain / pathology
  • Cell Membrane / genetics
  • Cell Membrane / metabolism*
  • Cell Membrane / pathology
  • Disease Models, Animal
  • Female
  • Male
  • Membrane Fluidity*
  • Mice
  • Mice, Transgenic
  • Oxidative Stress / genetics
  • Spinal Cord / metabolism*
  • Spinal Cord / pathology
  • Superoxide Dismutase / genetics
  • Superoxide Dismutase / metabolism
  • Superoxide Dismutase-1


  • Sod1 protein, mouse
  • Superoxide Dismutase
  • Superoxide Dismutase-1