Experience-dependent synaptic plasticity in V1 occurs without microglial CX3CR1
Name
10541.full.pdf
Size
1.74 MB
Format
Adobe PDF
Checksum (MD5)
366244c054c51f877f8de81d5744a821
Author(s)
Maher, Erin E.
Welsh, Christina A.
Stevens, Beth
Erisir, Alev
Schecter, Rachel Ward
Bear, Mark
Date Issued
November 2017
Journal
Journal of Neuroscience
Publisher
Society for Neuroscience
Citation
Schecter, Rachel W. et al. “Experience-Dependent Synaptic Plasticity in V1 Occurs Without Microglial CX3CR1.” The Journal of Neuroscience (September 2017): 2679–16 © 2017 The Authors
Version
Final published version
Abstract
Brief monocular deprivation (MD) shifts ocular dominance and reduces the density of thalamic synapses in layer 4 of the mouse primary visual cortex (V1). We found that microglial lysosome content is also increased as a result of MD. Previous studies have shown that the microglial fractalkine receptor CX3CR1 is involved in synaptic development and hippocampal plasticity.Wetherefore tested the hypothesis that neuron-to-microglial communication via CX3CR1 is an essential component of visual cortical development and plasticity in male mice. Our data show that CX3CR1 is not required for normal development of V1 responses to visual stimulation, multiple forms of experience-dependent plasticity, or the synapse loss that accompanies MD in layer 4. By ruling out an essential role for fractalkine signaling, our study narrows the search for understanding how microglia respond to active synapse modification in the visual cortex. Keywords: microglia; ocular dominance plasticity; stimulus-selective response potentiation; synaptic plasticity; visual cortex
MIT Department
Picower Institute for Learning and Memory
Terms of Use
Attribution 4.0 International (CC BY 4.0)
Persistent DSpace Link
DOI of Published Version
https://doi.org/10.1523/JNEUROSCI.2679-16.2017
