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

NEUROSCIENCE LETTERS

卷:219

Article

Jaarsma, D ; Holstege, JC ; Troost, D ; Davis, M ; Kennis, J ; Haasdijk, ED ; deJong, VJMB

关键词: immediate early genes;    spinal interneurons;    motoneuron disease;    reticular formation;   

DOI  :  10.1016/S0304-3940(96)13202-X

来源: Elsevier

【 摘 要 】

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 Endings are of interest since increased levels of c-jun also have been found in the intermediate zone of the spinal cord of ALS patients. Thus c-Jun may be involved in the neurodegenerative processes both in ALS and in motoneuron disease in SOD1(G93A) mice.

【 授权许可】

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