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Arc mediates intercellular synaptic plasticity via IRSp53-dependent extracellular vesicle biogenesis.

Ravens, A.; Sullivan, K.; Einstein, J.; Keceli, S. K.; Kicmal, T.; Tyagi, M.; Hantak, M. P.; Shepherd, T.; Stewart, A.; Lyon, K.; Dharan, A.; Gallagher, T.; Campbell, E. M.; Shepherd, J. D.

2024-01-30 neuroscience
10.1101/2024.01.30.578027 bioRxiv
Show abstract

Current models of learning and memory have focused on cell-autonomous regulation of synaptic strength; however, intercellular signaling between cells in the brain is critical for normal cognition. The immediate early gene Arc is a repurposed retrotransposon critical for long-term forms of synaptic plasticity and memory. Arc protein forms virus-like capsids released in extracellular vesicles (EVs) that signal cell-to-cell. Here, we find that long-term potentiation (LTP) stimuli induce the biogenesis of Arc EVs by recruiting the I-BAR protein IRSp53 to dendrites, which facilitates Arc capsid assembly and release. Arc EVs transfer Arc protein and mRNA to neighboring neurons, where translation of transferred Arc mRNA induces a loss of surface AMPA-type glutamate receptors. These results show that Arc EVs mediate non-cell autonomous long-term depression (LTD), revealing an intercellular form of synaptic plasticity that may be critical for memory consolidation.

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