Klein R
European Molecular Biology Laboratory, Differentiation Programme, Heidelberg, Germany.
FASEB J. 1994 Jul;8(10):738-44. doi: 10.1096/fasebj.8.10.8050673.
During vertebrate development, naturally occurring neuronal cell death is regulated by target-derived peptide factors, called neurotrophins. A recent series of papers describe the phenotypes of germline-targeted mutant mice deficient in neurotrophins and their receptors. Histological analysis of these mice for the first time has provided knowledge about the specific neuron populations that are dependent on neurotrophin action for development. Mice deficient for nerve growth factor (NGF) and its high-affinity receptor, encoded by the trkA proto-oncogene, suffer from complete loss of sympathetic neurons and sensory neurons responsive to temperature and pain. Mice deficient for brain-derived neurotrophic factor (BDNF) and its receptor, encoded by the trkB gene, display loss of sensory neurons responsive to tactile stimuli. In addition, trkB mutant mice experience loss of motor neurons indicating a possible specific function of the second TrkB ligand, neurotrophin-4 (NT-4), in motor neuron development. Mice deficient for neurotrophin-3 (NT-3) and its receptor, encoded by the trkC gene, show abnormal movements caused by the loss of sensory proprioceptive neurons.
在脊椎动物发育过程中，自然发生的神经元细胞死亡受称为神经营养因子的靶源性肽因子调控。最近一系列论文描述了缺乏神经营养因子及其受体的种系靶向突变小鼠的表型。对这些小鼠的组织学分析首次提供了有关依赖神经营养因子作用进行发育的特定神经元群体的知识。缺乏神经生长因子（NGF）及其由trkA原癌基因编码的高亲和力受体的小鼠，会完全丧失交感神经元以及对温度和疼痛有反应的感觉神经元。缺乏脑源性神经营养因子（BDNF）及其由trkB基因编码的受体的小鼠，表现出对触觉刺激有反应的感觉神经元丧失。此外，trkB突变小鼠会出现运动神经元丧失，这表明第二种TrkB配体神经营养因子-4（NT-4）在运动神经元发育中可能具有特定功能。缺乏神经营养因子-3（NT-3）及其由trkC基因编码的受体的小鼠，会因感觉本体感觉神经元丧失而出现异常运动。
