In vivo imaging reveals rapid morphological reactions of astrocytes towards focal lesions in an ALS mouse model

Neurosci Lett. 2011 Jun 22;497(2):148-51. doi: 10.1016/j.neulet.2011.04.049. Epub 2011 Apr 27.

Abstract

Pathophysiology of the motoneuron disease amyotrophic lateral sclerosis (ALS) is non-cell-autonomous. In mouse models of familiar ALS, neurotoxicity is derived not only from mutant motor neurons but also from mutant neighbouring glial cells. In vivo imaging by two-photon laser-scanning microscopy was used to study rapid morphological reactions of astroglial cells towards laser-induced axonal transection in ALS-linked transgenic SOD1(G93A) mice. In the affected lateral spinal cord, mutated astroglial cells extended branches towards injured axons within a time frame of minutes to hours post lesion while in control animals astrocytes lack any rapid morphological alteration within the studied time frame. This suggests that astrocytes partially contribute to the rapid response of non-neuronal cells to acute axonal lesions in ALS mice.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Amyotrophic Lateral Sclerosis / genetics
  • Amyotrophic Lateral Sclerosis / pathology*
  • Animals
  • Astrocytes / pathology*
  • Axons / pathology*
  • Cell Communication / physiology*
  • Disease Models, Animal
  • Mice
  • Mice, Transgenic
  • Microglia / pathology
  • Microscopy, Confocal / methods
  • Motor Neurons / pathology*
  • Spinal Cord / pathology
  • Superoxide Dismutase / genetics
  • Superoxide Dismutase-1

Substances

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