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MicroRNA miR124 is required for the expression of homeostatic synaptic plasticity

Author

Listed:
  • Qingming Hou

    (Boston University)

  • Hongyu Ruan

    (New England Primate Research Center, Harvard Medical School)

  • James Gilbert

    (Boston University)

  • Guan Wang

    (Boston University)

  • Qi Ma

    (New England Primate Research Center, Harvard Medical School)

  • Wei-Dong Yao

    (New England Primate Research Center, Harvard Medical School)

  • Heng-Ye Man

    (Boston University
    Boston University)

Abstract

Homeostatic synaptic plasticity is a compensatory response to alterations in neuronal activity. Chronic deprivation of neuronal activity results in an increase in synaptic AMPA receptors (AMPARs) and postsynaptic currents. The biogenesis of GluA2-lacking, calcium-permeable AMPARs (CP-AMPARs) plays a crucial role in the homeostatic response; however, the mechanisms leading to CP-AMPAR formation remain unclear. Here we show that the microRNA, miR124, is required for the generation of CP-AMPARs and homeostatic plasticity. miR124 suppresses GluA2 expression via targeting its 3′-UTR, leading to the formation of CP-AMPARs. Blockade of miR124 function abolishes the homeostatic response, whereas miR124 overexpression leads to earlier induction of homeostatic plasticity. miR124 transcription is controlled by an inhibitory transcription factor EVI1, acting by association with the deacetylase HDAC1. Our data support a cellular cascade in which inactivity relieves EVI1/HDAC-mediated inhibition of miR124 gene transcription, resulting in enhanced miR124 expression, formation of CP-AMPARs and subsequent induction of homeostatic synaptic plasticity.

Suggested Citation

  • Qingming Hou & Hongyu Ruan & James Gilbert & Guan Wang & Qi Ma & Wei-Dong Yao & Heng-Ye Man, 2015. "MicroRNA miR124 is required for the expression of homeostatic synaptic plasticity," Nature Communications, Nature, vol. 6(1), pages 1-12, December.
    • Handle: RePEc:nat:natcom:v:6:y:2015:i:1:d:10.1038_ncomms10045
    DOI: 10.1038/ncomms10045
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