You are here

J Neurosci DOI:10.1523/JNEUROSCI.2679-16.2017

Experience-Dependent Synaptic Plasticity in V1 Occurs without Microglial CX3CR1.

Publication TypeJournal Article
Year of Publication2017
AuthorsSchecter, RW, Maher, EE, Welsh, CA, Stevens, B, Erisir, A, Bear, MF
JournalJ Neurosci
Date Published2017 11 01
KeywordsAnimals, Cell Communication, CX3C Chemokine Receptor 1, Evoked Potentials, Visual, Geniculate Bodies, Male, Mice, Mice, 129 Strain, Mice, Inbred C57BL, Mice, Knockout, Mice, Transgenic, Microglia, Neuronal Plasticity, Organ Culture Techniques, Receptors, Chemokine, Vision, Monocular, Visual Cortex

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. We therefore 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. Microglia in the visual cortex respond to monocular deprivation with increased lysosome content, but signaling through the fractalkine receptor CX3CR1 is not an essential component in the mechanisms of visual cortical development or experience-dependent synaptic plasticity.


Alternate JournalJ. Neurosci.
PubMed ID28951447
PubMed Central IDPMC5666579
Grant ListR01 EY012309 / EY / NEI NIH HHS / United States
U54 HD090255 / HD / NICHD NIH HHS / United States