当前位置: X-MOL 学术IUBMB Life › 论文详情
Our official English website, www.x-mol.net, welcomes your feedback! (Note: you will need to create a separate account there.)
Actin remodeling, the synaptic tag and the maintenance of synaptic plasticity
IUBMB Life ( IF 4.6 ) Pub Date : 2020-02-20 , DOI: 10.1002/iub.2261
Júlia Pinho 1 , Cristina Marcut 1 , Rosalina Fonseca 1
Affiliation  

Activity‐dependent plasticity of synaptic connections is a hallmark of the mammalian brain and represents a key mechanism for rewiring neural circuits during development, experience‐dependent plasticity, and brain disorders. Cellular models of memory, such as long‐term potentiation and long‐term depression, share common principles to memory consolidation. As for memory, the maintenance of synaptic plasticity is dependent on the synthesis of de novo protein synthesis. The synaptic‐tagging and capture hypothesis states that the maintenance of synaptic plasticity is dependent on the interplay between input‐specific synaptic tags and the allocation or capture of plasticity‐related proteins (PRPs) at activated synapses. The setting of the synaptic tag and the capture of PRPs are independent processes that can occur separated in time and different groups of activated synapses. How are these two processes orchestrated in time and space? Here, we discuss the synaptic‐tagging and capture hypothesis in the light of neuronal compartmentalization models and address the role of actin as a putative synaptic tag. If different groups of synapses interact by synaptic‐tagging and capture mechanisms, understanding the spatial rules of such interaction is key to define the relevant neuronal compartment. We also discuss how actin modulation can allow an input‐specific capture of PRPs and try to conciliate the temporal dynamics of synaptic actin with the maintenance of plasticity. Understanding how multiple synapses interact in time and space is fundamental to predict how neurons integrate information and ultimately how memory is acquired.

中文翻译:

肌动蛋白重塑、突触标签和突触可塑性的维持

突触连接的活动依赖性可塑性是哺乳动物大脑的标志,代表了在发育、经验依赖性可塑性和脑部疾病期间重新连接神经回路的关键机制。记忆的细胞模型,例如长时程增强和长时程抑制,共享记忆巩固的共同原则。至于记忆,突触可塑性的维持依赖于蛋白质从头合成的合成。突触标记和捕获假说指出,突触可塑性的维持取决于输入特异性突触标签与激活突触处可塑性相关蛋白 (PRP) 的分配或捕获之间的相互作用。突触标签的设置和 PRP 的捕获是独立的过程,可以在时间上分开发生,并且可以在不同的激活突触组中发生。这两个过程是如何在时间和空间上编排的?在这里,我们根据神经元区室化模型讨论突触标记和捕获假设,并解决肌动蛋白作为推定突触标记的作用。如果不同的突触组通过突触标记和捕获机制相互作用,那么了解这种相互作用的空间规则是定义相关神经元区室的关键。我们还讨论了肌动蛋白调节如何允许输入特定的 PRP 捕获,并尝试协调突触肌动蛋白的时间动态与可塑性的维持。
更新日期:2020-02-20
down
wechat
bug