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Experience-Dependent Synaptic Plasticity in V1 Occurs without Microglial CX3CR1
Rachel W Schecter1, Erin E Maher2, Christina A Welsh3
1Picower Institute for Learning and Memory, Massachusetts Institute of Technology, Cambridge, Massachusetts 02139.
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. 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.SIGNIFICANCE STATEMENT 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.
Insights
Microglia in the visual cortex increase lysosome content after brief monocular deprivation. However, neuron-to-microglial communication via CX3CR1 is not essential for visual cortical development or plasticity.
Area of Science:
- Neuroscience
- Neurobiology
- Visual System Development
Background:
- Monocular deprivation (MD) alters visual cortex ocular dominance and synaptic density.
- Microglia, the brain's immune cells, show increased lysosome content after MD.
- The fractalkine receptor CX3CR1 mediates neuron-microglia communication and is implicated in plasticity.
Purpose of the Study:
- To investigate the role of neuron-to-microglial CX3CR1 signaling in visual cortical development and plasticity.
- To determine if CX3CR1 is essential for synaptic changes and functional adaptations following MD.
Main Methods:
- Utilized male mice lacking the CX3CR1 gene (knockout mice).
- Assessed visual cortical responses to visual stimulation.
- Examined experience-dependent plasticity and synapse loss in response to MD.
Main Results:
- CX3CR1 signaling is not required for normal development of primary visual cortex (V1) responses.
- Absence of CX3CR1 did not impair experience-dependent plasticity or MD-induced synapse loss.
- Microglial lysosome content increased with MD, independent of CX3CR1.
Conclusions:
- Fractalkine signaling via CX3CR1 is not essential for visual cortical development or plasticity in mice.
- This study excludes a critical role for CX3CR1 in microglial responses to synaptic modification during visual development.
- Narrows the focus for future research into microglial mechanisms underlying visual cortex plasticity.
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