Yuen E C, Howe C L, Li Y, Holtzman D M, Mobley W C
Department of Neurology, University of California at San Francisco 94143, USA.
Brain Dev. 1996 Sep-Oct;18(5):362-8. doi: 10.1016/0387-7604(96)00051-4.
The discovery of nerve growth factor (NGF) over 40 years ago led to the formulation of the "Neurotrophic Factor Hypothesis". This hypothesis states that developing neurons compete with each other for a limited supply of a neurotrophic factor (NTF) provided by the target tissue. Successful competitors survive; unsuccessful ones die. Subsequent research on NTFs has shown that NTF expression and actions are considerably more complex and diverse than initially predicted. Even for NGF, different regulatory patterns are seen for different neuronal populations. As would be predicted by the "Neurotrophic Factor Hypothesis", NGF levels critically regulate basal forebrain cholinergic neuron size and neurochemical differentiation. In contrast, the level of trkA, the NGF receptor, regulates these properties in caudate-putamen cholinergic neurons. Understanding NTF regulation and actions on neurons has led to their use in clinical trials of human neurological diseases. NTFs may emerge as important therapies to prevent neuronal dysfunction and death.
40多年前神经生长因子（NGF）的发现催生了“神经营养因子假说”。该假说认为，发育中的神经元相互竞争，以获取由靶组织提供的有限神经营养因子（NTF）。成功的竞争者存活下来，失败的则死亡。随后对NTF的研究表明，NTF的表达和作用比最初预测的要复杂和多样得多。即使是对于NGF，不同的神经元群体也有不同的调节模式。正如“神经营养因子假说”所预测的那样，NGF水平严格调节基底前脑胆碱能神经元的大小和神经化学分化。相比之下，NGF受体trkA的水平调节尾状核-壳核胆碱能神经元的这些特性。了解NTF对神经元的调节和作用已促使其用于人类神经系统疾病的临床试验。NTF可能成为预防神经元功能障碍和死亡的重要疗法。
