p75神经营养因子受体在体内影响交感神经元对NT-3的反应性。
The p75 neurotrophin receptor influences NT-3 responsiveness of sympathetic neurons in vivo.
作者信息
Brennan C, Rivas-Plata K, Landis S C
机构信息
Neural Development Section, National Institutes of Neurological Disorders and Stroke, National Institutes of Health, 36 Convent Dr., Bldg. 36/Rm. 2B08, Bethesda, Maryland 20892-4064, USA.
出版信息
Nat Neurosci. 1999 Aug;2(8):699-705. doi: 10.1038/11158.
To determine the role of the p75 neurotrophin receptor (p75NTR) in sympathetic neuron development, we crossed transgenic mice with mutations in p75NTR, nerve growth factor (NGF) and neurotrophin-3 (NT-3). Neuron number is normal in sympathetic ganglia of adult p75NTR-/- mice. Mice heterozygous for a NGF deletion (NGF+/-) have 50% fewer sympathetic neurons. In the absence of p75NTR (p75NTR-/- NGF+/-), however, neuron number is restored to wild-type levels. When NT-3 levels are reduced (p75NTR-/- NGF+/- NT3 +/-), neuron number decreases compared to p75NTR-/- NGF+/- NT3+/+. Thus, without p75NTR, NT3 substitutes for NGF, suggesting that p75 alters the neurotrophin specificity of TrkA in vivo.
为了确定p75神经营养因子受体（p75NTR）在交感神经元发育中的作用，我们将p75NTR、神经生长因子（NGF）和神经营养因子-3（NT-3）发生突变的转基因小鼠进行杂交。成年p75NTR-/-小鼠交感神经节中的神经元数量正常。NGF缺失杂合子（NGF+/-）小鼠的交感神经元数量减少50%。然而，在没有p75NTR的情况下（p75NTR-/- NGF+/-），神经元数量恢复到野生型水平。当NT-3水平降低时（p75NTR-/- NGF+/- NT3 +/-），与p75NTR-/- NGF+/- NT3+/+相比，神经元数量减少。因此，在没有p75NTR的情况下，NT3可替代NGF，这表明p75在体内改变了TrkA的神经营养因子特异性。
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