Piochon Claire, Kano Masanobu, Hansel Christian
Department of Neurobiology, University of Chicago, Chicago, Illinois, USA.
Department of Physiology, Northwestern University, Chicago, Illinois, USA.
Nat Neurosci. 2016 Sep 27;19(10):1299-310. doi: 10.1038/nn.4389.
In long-term depression (LTD) at synapses in the adult brain, synaptic strength is reduced in an experience-dependent manner. LTD thus provides a cellular mechanism for information storage in some forms of learning. A similar activity-dependent reduction in synaptic strength also occurs in the developing brain and there provides an essential step in synaptic pruning and the postnatal development of neural circuits. Here we review evidence suggesting that LTD and synaptic pruning share components of their underlying molecular machinery and may thus represent two developmental stages of the same type of synaptic modulation that serve different, but related, functions in neural circuit plasticity. We also assess the relationship between LTD and synaptic pruning in the context of recent findings of LTD dysregulation in several mouse models of autism spectrum disorder (ASD) and discuss whether LTD deficits can indicate impaired pruning processes that are required for proper brain development.
在成人大脑的突触处发生的长期抑制(LTD)过程中,突触强度以依赖于经验的方式降低。因此,LTD为某些形式的学习中的信息存储提供了一种细胞机制。在发育中的大脑中也会出现类似的依赖于活动的突触强度降低,这为突触修剪和神经回路的出生后发育提供了关键步骤。在这里,我们回顾了相关证据,这些证据表明LTD和突触修剪共享其潜在分子机制的组成部分,因此可能代表了同一类型突触调制的两个发育阶段,它们在神经回路可塑性中发挥着不同但相关的功能。我们还根据最近在几种自闭症谱系障碍(ASD)小鼠模型中发现的LTD失调情况,评估LTD与突触修剪之间的关系,并讨论LTD缺陷是否可能表明正常大脑发育所需的修剪过程受损。