Laboratory for Neurobiology of Memory, P.K. Anokhin Research Institute of Normal Physiology, Baltiyskaya 8, Moscow, 125315, Russian Federation.
Wave Processes and Control Systems Laboratory, Moscow Institute of Physics and Technology, Institutskiy per. 9, Dolgoprudny, Moscow Region, 141701, Russian Federation.
Neurosci Biobehav Rev. 2019 Apr;99:275-281. doi: 10.1016/j.neubiorev.2019.02.006. Epub 2019 Feb 14.
Stabilization of neuronal plastic changes is mediated by transient gene expression, including transcription of the activity-regulated cytoskeleton-associated gene (Arc), also known as Arg 3.1. Arc is implicated in several types of synaptic plasticity, including synaptic scaling, long-term potentiation, and long-term depression. However, the precise mechanisms by which Arc mediates these forms of long-term plasticity are unclear. It was recently found that Arc protein is capable of forming capsid-like structures and of transferring its own mRNA to neighboring cells. Moreover, Arc mRNA undergoes activity-dependent translation in these "transfected" cells. These new data raise unexpected possibilities for the mechanisms of the Arc action, and many intriguing questions concerning the role of Arc transcellular traffic in neuronal plasticity. In this mini-review, we discuss a possible link between the role of Arc in learning and memory and the virus-like properties of this protein. Additionally, we highlight some of the emerging questions for future neurobiological studies and translational applications of Arc transsynaptic effects.
神经元可塑性的稳定是通过瞬时基因表达介导的，包括活性调节细胞骨架相关基因 (Arc)，也称为 Arg 3.1 的转录。Arc 参与多种类型的突触可塑性，包括突触缩放、长时程增强和长时程抑制。然而，Arc 介导这些形式的长期可塑性的确切机制尚不清楚。最近发现，Arc 蛋白能够形成衣壳样结构，并将其自身的 mRNA 转移到邻近细胞。此外，Arc mRNA 在这些“转染”细胞中经历活性依赖性翻译。这些新数据为 Arc 作用的机制提出了意想不到的可能性，并且围绕 Arc 细胞间运输在神经元可塑性中的作用提出了许多有趣的问题。在这篇小综述中，我们讨论了 Arc 在学习和记忆中的作用与该蛋白的病毒样特性之间可能存在的联系。此外，我们还强调了未来神经生物学研究和 Arc 跨突触效应转化应用中出现的一些新问题。
