Induction of c-Jun immunoreactivity in spinal cord and brainstem neurons in a transgenic mouse model for amyotrophic lateral sclerosis

Neurosci Lett. 1996 Nov 29;219(3):179-82. doi: 10.1016/s0304-3940(96)13202-x.


Transgenic mice carrying amyotrophic lateral sclerosis (ALS)-linked superoxide dismutase 1 (SOD1) mutations develop a motoneuron disease resembling human ALS. c-Jun is a transcription factor frequently induced in injured neurons. In this study we have examined the distribution of c-Jun-immunoreactivity in the brainstem and spinal cord of transgenic SOD1 mice with a glycine 93 alanine (G93A) mutation. In non-transgenic littermates c-Jun immunostaining was predominantly situated in motoneurons. The number of c-Jun immunoreactive motoneuron was reduced in SOD1(G93A) mice due to pronounced loss of motoneurons. In SOD1(G93A) mice, however, c-Jun-immunoreactivity was strongly induced in neurons in the intermediate zone (Rexed's laminae V-VIII and X) of the spinal cord and throughout the brainstem reticular formation. These findings are of interest since increased levels of c-jun also have been found in the intermediate zone of the spinal cord of ALS patients. This c-Jun may be involved in the neurodegenerative processes both in ALS and in motoneuron disease in SOD1(G93A) mice.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Amyotrophic Lateral Sclerosis / genetics
  • Amyotrophic Lateral Sclerosis / metabolism*
  • Animals
  • Brain Stem / cytology
  • Brain Stem / metabolism*
  • Immunologic Techniques
  • Isoenzymes / genetics
  • Mice
  • Mice, Transgenic
  • Motor Neurons / metabolism
  • Mutation
  • Neurons / metabolism*
  • Proto-Oncogene Proteins c-jun / metabolism*
  • Spinal Cord / cytology
  • Spinal Cord / metabolism*
  • Superoxide Dismutase / genetics
  • Tissue Distribution


  • Isoenzymes
  • Proto-Oncogene Proteins c-jun
  • Superoxide Dismutase