Microglia: Dynamic Mediators of Synapse Development and Plasticity
Open accessAbstract
Neuronal communication underlies all brain activity and the genesis of complex behavior. Emerging research has revealed an unexpected role for immune molecules in the development and plasticity of neuronal synapses. Moreover microglia, the resident immune cells of the brain, express and secrete immune-related signaling molecules that alter synaptic transmission and plasticity in the absence of inflammation. When inflammation does occur, microglia modify synaptic connections and synaptic plasticity required for learning and memory. Here we review recent findings demonstrating how the dynamic interactions between neurons and microglia shape the circuitry of the nervous system in the healthy brain and how altered neuron-microglia signaling could contribute to disease.
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Microglia carry out key functions in brain development, including circuit refinement, neurogenesis, and neuronal growth.
“It is well established that microglia perform key functions in the development of the brain such as in circuit refinement, neurogenesis, and neuronal growth 39.”
From Efficient derivation of microglia-like cells from human pluripotent stem cells (2016) · cites this paper as [39]
Microglia have the capacity to monitor neuronal activity and modulate synaptic plasticity.
“This grants microglia the capacity to monitor neuronal activity and modulate synaptic plasticity22.”
From Interplay between innate immunity and Alzheimer disease: APOE and TREM2 in the spotlight (2018) · cites this paper as [22]
Microglia can regulate synapses through contact-dependent mechanisms, including engulfment of synaptic elements.
“Recent studies have revealed that microglia can also regulate synapses through contact-dependent mechanisms, including engulfment of synaptic elements”
From Glia-to-neuron transfer of miRNAs via extracellular vesicles: a new mechanism underlying inflammation-induced synaptic alterations (2018) · cites this paper as [82]
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- Authors
- Wu, Y., Dissing-Olesen, L., MacVicar, B. A., & Stevens, B.
- Affiliations
- Boston Children's Hospital (US)
- University of British Columbia (CA)
- Corresponding author
- Stevens, Beth
- Venue
- Trends in Immunology
- Publisher
- Elsevier BV
- Published
- 2015-10
- Volume
- 36
- Issue
- 10
- Pages
- 605-613
- ISSN
- 1471-4906 (ISSN-L)
- PMC
- PMC4841266
- OpenAlex
- W2152914442
- Cited by
- 661
- References
- 61
- Citations by year
- 2026: 31 · 2025: 42 · 2024: 51 · 2023: 66 · 2022: 78 · 2021: 94 · 2020: 71 · 2019: 84 · 2018: 65 · 2017: 45 · 2016: 34
- FWCI
- 3.76
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Trends in Immunology (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- Lundbeckfonden (R182-2014-2844)
- National Institute of Neurological Disorders and Stroke (R01NS084298, R01NS071008)
- 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 development, synaptic plasticity, microglia-neuron interaction, neuroinflammation, synaptic transmission, learning and memory, brain development, neurodegenerative diseases
- MeSH terms
- Aging, Animals, Brain, Central Nervous System, Humans, Inflammation, Neuronal Plasticity, Synapses, Neuroimmunomodulation, Signal Transduction, Microglia
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