December 2019
Volume 19, Issue 15
Open Access
OSA Fall Vision Meeting Abstract  |   December 2019
Microglial mechanisms of experience-dependent plasticity in the mouse visual cortex
Author Affiliations
  • Ania K. Majewska
    University of Rochester
Journal of Vision December 2019, Vol.19, 18. doi:
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      Ania K. Majewska; Microglial mechanisms of experience-dependent plasticity in the mouse visual cortex. Journal of Vision 2019;19(15):18.

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      © ARVO (1962-2015); The Authors (2016-present)

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The ability to tune synapses, and thus alter neural networks, is critical to both the normal development of brain circuitry and brain function throughout life, underlying processes such as learning and memory. Microglia are immune cells that infiltrate the brain early in development before the formation of the blood brain barrier. They have critical roles during brain injury, infection or disease. However, new data has thrust these non-neural cells into the spotlight as regulators of synapses. In the absence of pathology, microglia display dynamic interactions with synapses, and contribute to experience-dependent plasticity in the visual cortex in vivo. Manipulations of visual experience elicit a remarkably rapid behavioral response in microglia which is distinct from their inflammatory response, and includes an increase in phagocytosis that corresponds to the early phase of plasticity when synapses are lost in this model and when microglia increase their synaptic interactions. Our recent work has focused on identifying the molecular mechanisms through which microglia respond to changes in neuronal activity and communicate with synapses. We show that push-pull mechanisms allow microglial dynamics to be regulated by behavioral state through microglial receptors that sense purine and norepinephrine release. These opposing pathways impact microglial interactions with neurons and change the remodeling of neuronal networks with experience. Our findings suggest that microglia play an important role in synaptic plasticity, and use a subset of their pathological molecular repertoire to implement plastic changes in the non-pathological brain.


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