PG Neuroplasticity, Leibniz Institute for Neurobiology, Brenneckestr.6, 39118 Magdeburg, Germany.
Adv Exp Med Biol. 2012;970:355-76. doi: 10.1007/978-3-7091-0932-8_16.
The communication between synapses and the cell nucleus has attracted considerable interest for many years. This interest is largely fueled by the idea that synapse-to-nucleus signaling might specifically induce the expression of genes that make long-term memory "stick." However, despite many years of research, it is still essentially unclear how synaptic signals are conveyed to the nucleus, and it remains to a large degree enigmatic how activity-induced gene expression feeds back to synaptic function. In this chapter, we will focus on the activity-dependent synapto-nuclear trafficking of protein messengers and discuss the underlying mechanisms of their retrograde transport and their supposed functional role in neuronal plasticity.
突触和细胞核之间的通讯多年来引起了相当大的兴趣。这种兴趣在很大程度上是基于这样一种观点，即突触到细胞核的信号传递可能特异性地诱导长期记忆“黏附”的基因表达。然而，尽管进行了多年的研究，但突触信号如何传递到细胞核仍然基本上不清楚，活动诱导的基因表达如何反馈到突触功能仍然在很大程度上是神秘的。在本章中，我们将重点讨论蛋白信使的活性依赖性突触核转运，并讨论其逆行运输的潜在机制及其在神经元可塑性中的推测功能作用。
