Abstract
Learning induces gene expression and memory consolidation requires new protein synthesis. Many of these activity-induced genes are transcription factors. One of the exceptions is a key immediate early gene, Arc, which has been implicated in several forms of synaptic plasticity and is critical for long-term memory formation. Recently, Arc was discovered to have retroviral properties, such as the ability to form virus-like capsids, that were repurposed from an ancient retrotransposon. Arc capsids are released in extracellular vesicles that mediate intercellular communication. Here, we review Arc's role in synaptic plasticity and propose a model for how Arc mediates memory consolidation via a novel intercellular non-cell autonomous form of long-term depression.