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.
Keywords: Arc/Arg 3.1; Immediate early genes; Learning; Memory; Retroviral-like genes; Transcellular trafficking.
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