Induction of c-Jun immunoreactivity in spinal cord and brainstem neurons in a transgenic mouse model for amyotrophic lateral sclerosis.
Neurosci Lett
; 219(3): 179-82, 1996 Nov 29.
Article
in En
| MEDLINE
| ID: mdl-8971809
ABSTRACT
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.
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Collection:
01-internacional
Database:
MEDLINE
Main subject:
Spinal Cord
/
Brain Stem
/
Proto-Oncogene Proteins c-jun
/
Amyotrophic Lateral Sclerosis
/
Neurons
Type of study:
Prognostic_studies
Limits:
Animals
Language:
En
Journal:
Neurosci Lett
Year:
1996
Document type:
Article
Affiliation country:
Netherlands