Microglial P2Y12 is necessary for synaptic plasticity in mouse visual cortex

G O Sipe1,2, R L Lowery1,2, M-È Tremblay1

  • 1Department of Neuroscience, University of Rochester, 601 Elmwood Avenue, box 603, Rochester, New York 14642, USA.

Nature Communications
|March 8, 2016
PubMed

Insights

Microglia, the brain's immune cells, are crucial for ocular dominance plasticity. Disrupting the P2Y12 receptor in microglia blocks this experience-dependent brain plasticity during development.

Area of Science:

  • Neuroscience
  • Immunology
  • Developmental Biology

Background:

  • Microglia are brain-resident immune cells involved in neurophysiology and development.
  • Ocular dominance plasticity involves changes in visual cortex connections during a critical period.

Purpose of the Study:

  • To investigate the role of microglia in ocular dominance plasticity.
  • To explore the involvement of the P2Y12 receptor in microglial responses and plasticity.

Main Methods:

  • Monocular deprivation in adolescent mice.
  • Analysis of microglial morphology, motility, and synaptic interactions.
  • Genetic disruption of the P2Y12 receptor.

Main Results:

  • Microglia alter morphology, motility, and synaptic interactions during monocular deprivation.
  • Disruption of the P2Y12 receptor impairs microglial response to deprivation.
  • P2Y12 receptor disruption abrogates ocular dominance plasticity.

Conclusions:

  • Microglia are essential for ocular dominance plasticity.
  • The P2Y12 receptor mediates microglial functions critical for this plasticity.
  • Microglia actively shape experience-dependent brain plasticity.

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