DISRUPTION OF THE NEURATROPHIN-3 RECEPTOR GENE TRKC ELIMINATES LA MUSCLE AFFERENTS AND RESULTS IN ABNORMAL MOVEMENTS
DISRUPTION OF THE NEURATROPHIN-3 RECEPTOR GENE TRKC ELIMINATES LA MUSCLE AFFERENTS AND RESULTS IN ABNORMAL MOVEMENTS
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DOI：
10.1038/368249a0
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发表时间：
1994-03-17
期刊：
影响因子：
64.8
通讯作者：
BARBACID, M
中科院分区：
文献类型：
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作者：
KLEIN, R;SILOSSANTIAGO, I;BARBACID, M
TrkC基因(1，2)广泛表达于哺乳动物神经系统(3-5)，编码一系列酪氨酸蛋白激酶亚型，作为神经营养因子(2，6-8)家族中神经生长因子(NGF)家族成员的神经营养因子-3(NT3)的受体。其中一个亚型gp145(TrkC)/trkC K1在培养细胞(2，6-8)中介导NT3的营养特性。在这里，我们显示TrkC酪氨酸蛋白激酶受体缺陷的纯合子小鼠缺乏Ia肌肉向脊髓运动神经元的传入投射，并且在脊髓的背根和后柱中有较少的大的有髓轴突。这些小鼠表现出异常的动作和姿势，表明依赖NT3/TrkC的感觉神经元可能在本体感觉、位置感觉和肢体运动中发挥主要作用。
THE trkC gene(1,2) is expressed throughout the mammalian nervous system(3-5) and encodes a series of tyrosine protein kinase isoforms that serve as receptors for neurotrophin-3 (NT3), a member of the nerve growth factor (NGF) family of neurotrophic factors(2,6-8). One of these isoforms, gp145(trkC)/TrkC K1, mediates the trophic properties of NT3 in cultured Cells(2,6-8). Here we show that homozygous mice defective for TrkC tyrosine protein kinase receptors lack Ia muscle afferent projections to spinal motor neurons and have fewer large myelinated axons in the dorsal root and posterior columns of the spinal cord. These mice display abnormal movements and postures, indicating that NT3/TrkC-dependent sensory neurons may play a primary role in proprioception, the sense of position and movement of the limbs.