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Regulation of synaptic connectivity by glia.
Open accessAbstract
The human brain contains more than 100 trillion (10(14)) synaptic connections, which form all of its neural circuits. Neuroscientists have long been interested in how this complex synaptic web is weaved during development and remodelled during learning and disease. Recent studies have uncovered that glial cells are important regulators of synaptic connectivity. These cells are far more active than was previously thought and are powerful controllers of synapse formation, function, plasticity and elimination, both in health and disease. Understanding how signalling between glia and neurons regulates synaptic development will offer new insight into how the nervous system works and provide new targets for the treatment of neurological diseases.
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“Evidence now shows that astrocytes are directly involved in synaptic connections and control, ranging from ionic balance to the genesis and behavior of synapses”
From Interlaminar and varicose-projection astrocytes: toward a new understanding of the primate brain (2024) · cites this paper as Eroglu and Barres, 2010
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“The main mechanisms regulating these processes involved in plasticity are thought to be changes in the cell-surface delivery, retention and Ca 2+ -channel properties of the postsynaptic ionotropic glutamate receptors, AMPA receptors and NMDA ( N -methyl- D -aspartate) receptor”
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Presynaptic α2δ-3 is required for synaptic morphogenesis independent of its Ca2+ - channel functions
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BackgroundLysosomal Activity Associated with Developmental Axon Pruning
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Self-citation
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Neuroinflammation and microglial activation in Alzheimer disease: where do we go from here?
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Variation in cancer risk among tissues can be explained by the number of stem cell divisions
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“Astrocytes are derived from neural stem cells (79), whose proportion has been estimated to be ~0.”
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Diversity of astrocyte functions and phenotypes in neural circuits
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“Immature astrocytes secrete an array of cytokines and other molecules that promote synapse formation and synaptic plasticity (Allen & Barres 2005, Bolton & Eroglu 2009, Eroglu & Barres 2010).”
BackgroundSelf-citation
Metadata
- Authors
- Eroglu, C., & Barres, B. A.
- Affiliations
- Stanford Medicine (US)
- ORCID
- Barres, Ben A.
- Venue
- Nature
- Published
- 2010-11
- Volume
- 468
- Issue
- 7321
- Pages
- 223-231
- ISSN
- 0028-0836 (ISSN-L)
- 1476-4687
- PMC
- PMC4431554
- OpenAlex
- W1973477241
- Cited by
- 813
- References
- 104
- Citations by year
- 2026: 21 · 2025: 46 · 2024: 48 · 2023: 52 · 2022: 54 · 2021: 60 · 2020: 52 · 2019: 52 · 2018: 66 · 2017: 54 · 2016: 50 · 2015: 50 · 2014: 55 · 2013: 58 · 2012: 58
- FWCI
- 4.31
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Nature (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- RePEc: Research Papers in Economics (submittedVersion)
- Funders
- Alfred P. Sloan Foundation
- National Institute on Drug Abuse (R01DA015043)
- Topics
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Life Sciences › Neuroscience › Developmental Neuroscience › Neurogenesis and neuroplasticity mechanisms
- Keywords
- glial cells, synaptic connectivity, synaptogenesis, synaptic pruning, synaptic plasticity, synaptic development, learning, neurological disorders
- MeSH terms
- Animals, Axons, Central Nervous System Diseases, Drosophila melanogaster, Humans, Synaptic Transmission, Neuroglia, Synapses
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