Van der Zee C E, Ross G M, Riopelle R J, Hagg T
Department of Anatomy and Neurobiology, Tupper Building, Dalhousie University, Halifax, Nova Scotia B3H 4H7, Canada.
Science. 1996 Dec 6;274(5293):1729-32. doi: 10.1126/science.274.5293.1729.
The functions of the low-affinity p75 nerve growth factor receptor (p75(NGFR)) 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 p75(NGFR)-deficient mice or in normal mice systemically injected with a p75(NGFR)-inhibiting peptide. Control, but not p75(NGFR)-deficient, mice also had fewer cholinergic striatal interneurons. Apparently, p75(NGFR) mediates apoptosis of these developing neurons in the absence of TrkA, and modulation of p75(NGFR) can promote neuronal survival. Cholinergic basal forebrain neurons are involved in learning and memory.
在体内研究了低亲和力p75神经生长因子受体（p75(NGFR)）在中枢神经系统中的功能。在正常小鼠中，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15天之间死亡。这种损失在p75(NGFR)基因缺陷小鼠或全身注射p75(NGFR)抑制肽的正常小鼠中并未发生。对照小鼠（而非p75(NGFR)基因缺陷小鼠）的胆碱能纹状体中间神经元也较少。显然，在没有TrkA的情况下，p75(NGFR)介导这些发育中神经元的凋亡，并且对p75(NGFR)的调节可促进神经元存活。胆碱能基底前脑神经元参与学习和记忆。
