Reichardt Louis F
Neuroscience Program, Department of Physiology and Howard Hughes Medical Institute, University of California-San Francisco, 1550 Fourth Street, Rock Hall 284a, San Francisco, CA 94158, USA.
Philos Trans R Soc Lond B Biol Sci. 2006 Sep 29;361(1473):1545-64. doi: 10.1098/rstb.2006.1894.
Neurotrophins are a family of closely related proteins that were identified initially as survival factors for sensory and sympathetic neurons, and have since been shown to control many aspects of survival, development and function of neurons in both the peripheral and the central nervous systems. Each of the four mammalian neurotrophins has been shown to activate one or more of the three members of the tropomyosin-related kinase (Trk) family of receptor tyrosine kinases (TrkA, TrkB and TrkC). In addition, each neurotrophin activates p75 neurotrophin receptor (p75NTR), a member of the tumour necrosis factor receptor superfamily. Through Trk receptors, neurotrophins activate Ras, phosphatidyl inositol-3 (PI3)-kinase, phospholipase C-gamma1 and signalling pathways controlled through these proteins, such as the MAP kinases. Activation of p75NTR results in activation of the nuclear factor-kappaB (NF-kappaB) and Jun kinase as well as other signalling pathways. Limiting quantities of neurotrophins during development control the number of surviving neurons to ensure a match between neurons and the requirement for a suitable density of target innervation. The neurotrophins also regulate cell fate decisions, axon growth, dendrite growth and pruning and the expression of proteins, such as ion channels, transmitter biosynthetic enzymes and neuropeptide transmitters that are essential for normal neuronal function. Continued presence of the neurotrophins is required in the adult nervous system, where they control synaptic function and plasticity, and sustain neuronal survival, morphology and differentiation. They also have additional, subtler roles outside the nervous system. In recent years, three rare human genetic disorders, which result in deleterious effects on sensory perception, cognition and a variety of behaviours, have been shown to be attributable to mutations in brain-derived neurotrophic factor and two of the Trk receptors.
神经营养因子是一类密切相关的蛋白质家族,最初被鉴定为感觉神经元和交感神经元的存活因子,后来被证明可控制外周和中枢神经系统中神经元存活、发育和功能的许多方面。四种哺乳动物神经营养因子中的每一种都已被证明可激活原肌球蛋白相关激酶(Trk)家族受体酪氨酸激酶(TrkA、TrkB和TrkC)的三个成员中的一个或多个。此外,每种神经营养因子都会激活p75神经营养因子受体(p75NTR),它是肿瘤坏死因子受体超家族的成员。通过Trk受体,神经营养因子激活Ras、磷脂酰肌醇-3(PI3)-激酶、磷脂酶C-γ1以及由这些蛋白质控制的信号通路,如丝裂原活化蛋白激酶。p75NTR的激活会导致核因子-κB(NF-κB)和Jun激酶以及其他信号通路的激活。发育过程中神经营养因子数量的限制控制着存活神经元的数量,以确保神经元与合适的靶神经支配密度需求相匹配。神经营养因子还调节细胞命运决定、轴突生长、树突生长和修剪以及蛋白质表达,如离子通道、递质生物合成酶和神经肽递质,这些对于正常神经元功能至关重要。成年神经系统中需要持续存在神经营养因子,它们在其中控制突触功能和可塑性,并维持神经元存活、形态和分化。它们在神经系统之外也有额外的、更微妙的作用。近年来,已证明三种罕见的人类遗传疾病会对感觉、认知和多种行为产生有害影响,这些疾病可归因于脑源性神经营养因子和两种Trk受体的突变。