Defects in sensory nerve numbers and growth in mutant Kit and Steel mice

被引:17
作者
Lourenssen, S
Motro, B
Bernstein, A
Diamond, J
机构
[1] McMaster Univ, Dept Psychiat & Behav Neurosci, Hamilton, ON L8N 3Z5, Canada
[2] Mt Sinai Hosp, Samuel Lunenfeld Res Inst, Dept Fetal Hlth & Dev, Toronto, ON M5G 1X5, Canada
[3] Univ Toronto, Dept Mol & Med Genet, Toronto, ON M5S 1A8, Canada
关键词
axonal regeneration; c-Kit; NGF; collateral sprouting; DRG neurons; neuron survival; steel factor; stem cell factor; tyrosine kinase;
D O I
10.1097/00001756-200004270-00004
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
The roles in the nervous system of the receptor tyrosine kinase Kit and its ligand, Steel factor, are unclear. We have now found first, that sensory nerve populations are reduced in mutant Kit and Steel mice, implicating Steel-Kit interactions in neuronal development. Second, sensory axonal regeneration (which occurs independently of nerve growth factor, or NGF) is impaired, while collateral sprouting (NGF dependent) is normal. Therefore, there is a selective involvement of Kit signal transduction pathways in nerve growth; supporting this, in wild-type animals Kit was up-regulated in regenerating, but unchanged in sprouting, sensory neurons. The receptor tyrosine kinase Kit thus contrasts with the receptor tyrosine kinase trkA, which is activated by the sprouting stimulus (NGF) but not by the axonal regeneration signal. NeuroReport 11:1159-1165 (C) 2000 Lippincott Williams & Wilkins.
引用
收藏
页码:1159 / 1165
页数:7
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