A role for microglia in synaptic plasticity?
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Remodeling of brain circuits, including the formation, modification and elimination of synaptic structures, occurs throughout life as animals adapt to their environment. Until very recently, known mechanisms for experience-dependent synaptic plasticity had placed neurons and their structural interactions with astrocytes in the spotlight. However microglia, the immune cells of the brain, are very active even in the absence of pathological insults and their processes periodically contact dendritic spines and axon terminals in vivo.1-3 This intriguing behavior prompted us to explore, using electron microscopy and two-photon in vivo imaging in the primary visual cortex of juvenile mice, a possible role for quiescent microglia in the modification of synaptic structures.4 Our work uncovered subtle changes in the behavior of microglia during manipulations of visual experience including regulation of perisynaptic extracellular spaces, contact with subsets of structurally dynamic and transient dendritic spines, and phagocytic engulfment of intact synapses. Based on these results, here we further discuss three means of synapse modification or elimination that could be mediated by microglia in the context of normal experience-dependent plasticity.
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Microglia have been implicated as active participants in brain plasticity.
“Microglia have recently been implicated as active participants in brain plasticity per se (42–45).”
From Prolonged Period of Cortical Plasticity upon Redox Dysregulation in Fast-Spiking Interneurons (2015) · cites this paper as [45]
Increased neurogenesis in the hippocampus and subventricular zone does not necessarily translate into increased neuron numbers in basal ganglia circuitry within the striatum, cortex, or thalamus.
“The fact that exercise increases neurogenesis in the hippocampus and subventricular zone does not necessarily translate into the potential role of exercise in increasing neuron numbers in important basal ganglia circuitry within the striatum, cortex, or thalamus 123.”
From Exercise-enhanced neuroplasticity targeting motor and cognitive circuitry in Parkinson's disease (2013) · cites this paper as [123]
Exercise increases neurogenesis in the hippocampus and subventricular zone.
“The fact that exercise increases neurogenesis in the hippocampus and subventricular zone does not necessarily translate into the potential role of exercise in increasing neuron numbers in important basal ganglia circuitry within the striatum, cortex, or thalamus 123.”
From Exercise-enhanced neuroplasticity targeting motor and cognitive circuitry in Parkinson's disease (2013) · cites this paper as [123]
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- Authors
- Tremblay, M.-È., & Majewska, A. K.
- Affiliations
- University of Rochester (US)
- Corresponding author
- Tremblay, Marie-Ève
- Venue
- Communicative & Integrative Biology
- Publisher
- Informa UK Limited
- Published
- 2011-03
- Volume
- 4
- Issue
- 2
- Pages
- 220-222
- ISSN
- 1942-0889 (ISSN-L)
- PMC
- PMC3104585
- OpenAlex
- W2003215052
- Cited by
- 176
- References
- 26
- Citations by year
- 2025: 5 · 2024: 13 · 2023: 7 · 2022: 14 · 2021: 13 · 2020: 12 · 2019: 11 · 2018: 12 · 2017: 9 · 2016: 9 · 2015: 17 · 2014: 19 · 2013: 17 · 2012: 12
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- cc-by-nc
- Locations
- Communicative & Integrative Biology (publishedVersion, cc-by-nc)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Burroughs Wellcome Fund
- National Institutes of Health
- National Eye Institute (R01EY019277, P30EY001319)
- Topics
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
- Life Sciences › Neuroscience › Developmental Neuroscience › Neurogenesis and neuroplasticity mechanisms
- Keywords
- microglia, synaptic plasticity, experience-dependent plasticity, dendritic spines, synaptic pruning, phagocytosis, primary visual cortex, extracellular space, synaptic remodeling
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