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Microglial P2Y12 is necessary for synaptic plasticity in mouse visual cortex

Author

Listed:
  • G. O. Sipe

    (University of Rochester
    Neuroscience Graduate Program, University of Rochester)

  • R. L. Lowery,

    (University of Rochester
    Neuroscience Graduate Program, University of Rochester)

  • M-È Tremblay

    (University of Rochester
    Present address: Department of Molecular Medicine, Université Laval, and Axe Neurosciences, CRCHU de Québec-Université Laval, Quebec City, Canada.)

  • E. A. Kelly

    (University of Rochester)

  • C. E. Lamantia

    (University of Rochester)

  • A. K. Majewska

    (University of Rochester
    Neuroscience Graduate Program, University of Rochester)

Abstract

Microglia are the resident immune cells of the brain. Increasingly, they are recognized as important mediators of normal neurophysiology, particularly during early development. Here we demonstrate that microglia are critical for ocular dominance plasticity. During the visual critical period, closure of one eye elicits changes in the structure and function of connections underlying binocular responses of neurons in the visual cortex. We find that microglia respond to monocular deprivation during the critical period, altering their morphology, motility and phagocytic behaviour as well as interactions with synapses. To explore the underlying mechanism, we focused on the P2Y12 purinergic receptor, which is selectively expressed in non-activated microglia and mediates process motility during early injury responses. We find that disrupting this receptor alters the microglial response to monocular deprivation and abrogates ocular dominance plasticity. These results suggest that microglia actively contribute to experience-dependent plasticity in the adolescent brain.

Suggested Citation

  • G. O. Sipe & R. L. Lowery, & M-È Tremblay & E. A. Kelly & C. E. Lamantia & A. K. Majewska, 2016. "Microglial P2Y12 is necessary for synaptic plasticity in mouse visual cortex," Nature Communications, Nature, vol. 7(1), pages 1-15, April.
    • Handle: RePEc:nat:natcom:v:7:y:2016:i:1:d:10.1038_ncomms10905
    DOI: 10.1038/ncomms10905
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    Cited by:

    1. Péter Berki & Csaba Cserép & Zsuzsanna Környei & Balázs Pósfai & Eszter Szabadits & Andor Domonkos & Anna Kellermayer & Miklós Nyerges & Xiaofei Wei & Istvan Mody & Araki Kunihiko & Heinz Beck & He Ka, 2024. "Microglia contribute to neuronal synchrony despite endogenous ATP-related phenotypic transformation in acute mouse brain slices," Nature Communications, Nature, vol. 15(1), pages 1-24, December.
    2. Wanjie Wu & Yingzhu He & Yujun Chen & Yiming Fu & Sicong He & Kai Liu & Jianan Y. Qu, 2024. "In vivo imaging in mouse spinal cord reveals that microglia prevent degeneration of injured axons," Nature Communications, Nature, vol. 15(1), pages 1-17, December.
    3. Katia Monsorno & Kyllian Ginggen & Andranik Ivanov & An Buckinx & Arnaud L. Lalive & Anna Tchenio & Sam Benson & Marc Vendrell & Angelo D’Alessandro & Dieter Beule & Luc Pellerin & Manuel Mameli & Ros, 2023. "Loss of microglial MCT4 leads to defective synaptic pruning and anxiety-like behavior in mice," Nature Communications, Nature, vol. 14(1), pages 1-18, December.

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