Induction of c-Jun phosphorylation in spinal motoneurons in neonatal and adult rats following axonal injury

• Published in: Brain research 2010-03, Vol.1320, p.7-15
• Main Authors: Yuan, Qiuju, Hu, Bing, Wu, Yin, Chu, Tak-Ho, Su, Huanxin, Zhang, Weiming, So, Kwok-Fai, Lin, Zhixiu, Wu, Wutian
• Format: Article
• Language: English
• Subjects: Aging - metabolism; Animals; Animals, Newborn; Axonal injury; Axons - metabolism; Biological and medical sciences; Cell Count; Cell Death - physiology; Cell Survival - physiology; Development. Senescence. Regeneration. Transplantation; Disease Models, Animal; Female; Fundamental and applied biological sciences. Psychology; GAP-43 Protein - metabolism; Glial Cell Line-Derived Neurotrophic Factor - metabolism; Immunohistochemistry; Motoneuron; Motor Neurons - metabolism; Nerve Regeneration - physiology; Neurology; Neuronal death; Phosphorylation; Proto-Oncogene Proteins c-jun - metabolism; Rats; Rats, Sprague-Dawley; Regeneration; Spinal cord; Spinal Cord - metabolism; Spinal Nerves - injuries; Spinal Nerves - metabolism; Vertebrates: nervous system and sense organs
• ISSN: 0006-8993; 1872-6240
• DOI: 10.1016/j.brainres.2010.01.038

Abstract This study aims to address if phosphorylation of the transcription factor c-Jun is associated with lesion-induced death of spinal motoneurons, and if this cellular response is modulated by glial-cell-line-derived neurotrophic factor (GDNF). We found that after both distal axotomy and root avulsion, spinal motoneurons in neonatal rats expressed phosphorylated c-Jun (p-c-Jun) and almost all injured motoneurons in these animals died. Similarly, root avulsion in adult rats also induced p-c-Jun expression that preceded the loss of motoneurons. In contrast, neither motoneuron death nor p-c-Jun induction was found after distal axotomy of spinal nerves in adult rats. Application of GDNF after distal axotomy in the neonatal model prevented motoneuron death but did not alter the expression of p-c-Jun in the surviving motoneurons. We conclude that c-Jun phosphorylation correlates with the cellular events leading to motoneuron death and that its expression cannot be modulated by GDNF. We further showed that expression of p-c-Jun was not correlated with the expression of growth-associated protein-43 (GAP-43), whose expression was closely correlated both temporally and spatially with periods of axonal outgrowth, suggesting that p-c-Jun may not be related with axonal regeneration of injured motoneurons.