Bernardinelli Yann, Nikonenko Irina, Muller Dominique
Department of Basic Neurosciences, University of Geneva Medical School Geneva, Switzerland.
Front Neuroanat. 2014 Nov 3;8:123. doi: 10.3389/fnana.2014.00123. eCollection 2014.
Synaptic plasticity mechanisms are usually discussed in terms of changes in synaptic strength. The capacity of excitatory synapses to rapidly modify the membrane expression of glutamate receptors in an activity-dependent manner plays a critical role in learning and memory processes by re-distributing activity within neuronal networks. Recent work has however also shown that functional plasticity properties are associated with a rewiring of synaptic connections and a selective stabilization of activated synapses. These structural aspects of plasticity have the potential to continuously modify the organization of synaptic networks and thereby introduce specificity in the wiring diagram of cortical circuits. Recent work has started to unravel some of the molecular mechanisms that underlie these properties of structural plasticity, highlighting an important role of signaling pathways that are also major candidates for contributing to developmental psychiatric disorders. We review here some of these recent advances and discuss the hypothesis that alterations of structural plasticity could represent a common mechanism contributing to the cognitive and functional defects observed in diseases such as intellectual disability, autism spectrum disorders and schizophrenia.
突触可塑性机制通常是根据突触强度的变化来讨论的。兴奋性突触以活动依赖的方式快速改变谷氨酸受体膜表达的能力,通过在神经网络内重新分配活动,在学习和记忆过程中起着关键作用。然而,最近的研究也表明,功能可塑性特性与突触连接的重新布线和激活突触的选择性稳定有关。可塑性的这些结构方面有可能持续改变突触网络的组织,从而在皮质回路的布线图中引入特异性。最近的研究已经开始揭示一些构成这些结构可塑性特性基础的分子机制,突出了信号通路的重要作用,而这些信号通路也是导致发育性精神疾病的主要候选因素。我们在此回顾其中一些最新进展,并讨论这样一种假说,即结构可塑性的改变可能是导致在诸如智力障碍、自闭症谱系障碍和精神分裂症等疾病中观察到的认知和功能缺陷的共同机制。