To form and maintain extremely intricate and functional neural circuitry, mammalian neurons are typically endowed with highly arborized dendrites and a long axon. The synapses that link neurons to neurons or to other cells are numerous and often too remote for the cell body to make and deliver new proteins to the right place in time. Moreover, synapses undergo continuous activity-dependent changes in their number and strength, establishing the basis of neural plasticity. The innate dilemma is then how a highly complex neuron provides new proteins for its cytoplasmic periphery and individual synapses to support synaptic plasticity. Here, we review a growing body of evidence that local protein synthesis in discrete sites of the axon and presynaptic terminals plays crucial roles in synaptic plasticity, and that deregulation of this local translation system is implicated in various pathologies of the nervous system.

为了形成和维持极其复杂和功能性的神经回路，哺乳动物神经元通常具有高度乔木化的树突和长轴突。将神经元与神经元或其他细胞连接起来的突触数量众多，而且通常距离细胞体太远，无法及时制造新蛋白质并将其输送到正确的位置。此外，突触的数量和强度会发生持续的活动依赖性变化，这为神经可塑性奠定了基础。天生的困境是高度复杂的神经元如何为其细胞质外围和单个突触提供新的蛋白质以支持突触可塑性。在这里，我们回顾了越来越多的证据表明轴突和突触前末端离散位点的局部蛋白质合成在突触可塑性中起关键作用，