Survival of Cholinergic Forebrain Neurons in Developing p75NGFR-Deficient Mice
Survival of Cholinergic Forebrain Neurons in Developing p75NGFR-Deficient Mice
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DOI：
10.1126/science.274.5293.1729
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发表时间：
1996-12
期刊：
影响因子：
56.9
通讯作者：
C. Van der Zee;G. Ross;R. Riopelle;T. Hagg
中科院分区：
文献类型：
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作者：
C. Van der Zee;G. Ross;R. Riopelle;T. Hagg
本实验在活体上探讨了低亲和力p75神经生长因子受体（p75NGFR）在中枢神经系统中的功能。在正常小鼠中，大约25%的胆碱能基底前脑神经元不表达TrkA，并在出生后第6天至第15天死亡。这种损失在p75NGFR缺陷小鼠或全身注射p75NGFR抑制肽的正常小鼠中没有发生。对照组，但不是p75NGFR缺陷，小鼠也有较少的胆碱能纹状体中间神经元。显然，在缺乏TrkA的情况下，p75NGFR介导这些发育中的神经元的凋亡，并且p75NGFR的调节可以促进神经元的存活。胆碱能基底前脑神经元参与学习和记忆。
The functions of the low-affinity p75 nerve growth factor receptor (p75NGFR) in the central nervous system were explored in vivo. In normal mice, approximately 25 percent of the cholinergic basal forebrain neurons did not express TrkA and died between postnatal day 6 and 15. This loss did not occur in p75NGFR-deficient mice or in normal mice systemically injected with a p75NGFR-inhibiting peptide. Control, but not p75NGFR-deficient, mice also had fewer cholinergic striatal interneurons. Apparently, p75NGFR mediates apoptosis of these developing neurons in the absence of TrkA, and modulation of p75NGFR can promote neuronal survival. Cholinergic basal forebrain neurons are involved in learning and memory.