Inflammation, glutamate, and glia: a trio of trouble in mood disorders
Open accessAbstract
Increasing data indicate that inflammation and alterations in glutamate neurotransmission are two novel pathways to pathophysiology in mood disorders. The primary goal of this review is to illustrate how these two pathways may converge at the level of the glia to contribute to neuropsychiatric disease. We propose that a combination of failed clearance and exaggerated release of glutamate by glial cells during immune activation leads to glutamate increases and promotes aberrant extrasynaptic signaling through ionotropic and metabotropic glutamate receptors, ultimately resulting in synaptic dysfunction and loss. Furthermore, glutamate diffusion outside the synapse can lead to the loss of synaptic fidelity and specificity of neurotransmission, contributing to circuit dysfunction and behavioral pathology. This review examines the fundamental role of glia in the regulation of glutamate, followed by a description of the impact of inflammation on glial glutamate regulation at the cellular, molecular, and metabolic level. In addition, the role of these effects of inflammation on glia and glutamate in mood disorders will be discussed along with their translational implications.
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Astrocyte immune activation has downstream impacts on cellular glutamate uptake and calcium signaling.
“Previous work has also highlighted the downstream impacts of astrocyte immune activation on cellular glutamate uptake and calcium signaling (Agulhon et al., 2012; Haroon et al., 2017; Shigetom, et al., 2019; Vallejo-Illarramendi et al., 2006).”
From Sterol dysregulation in Smith–Lemli–Opitz syndrome causes astrocyte immune reactivity through microglia crosstalk (2022) · cites this paper as Haroon et al., 2017
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“Previous work has also highlighted the downstream impacts of astrocyte immune activation on cellular glutamate uptake and calcium signaling (Agulhon et al., 2012; Haroon et al., 2017; Shigetom, et al., 2019; Vallejo-Illarramendi et al., 2006).”
- Authors
- Haroon, E., Miller, A. H., & Sanacora, G.
- Affiliations
- Emory University (US)
- Yale University (US)
- Corresponding author
- Haroon, Ebrahim
- Venue
- Neuropsychopharmacology
- Published
- 2016-09-15
- Volume
- 42
- Issue
- 1
- Pages
- 193-215
- ISSN
- 0893-133X (ISSN-L)
- 1740-634X
- PMC
- PMC5143501
- OpenAlex
- W2519381186
- Cited by
- 584
- References
- 46
- Citations by year
- 2026: 82 · 2025: 85 · 2024: 84 · 2023: 74 · 2022: 66 · 2021: 63 · 2020: 57 · 2019: 34 · 2018: 27 · 2017: 11 · 2016: 1
- FWCI
- 1.46
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Neuropsychopharmacology (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- AstraZeneca
- State of Connecticut Department of Mental Health and Addiction Services
- National Alliance for Research on Schizophrenia and Depression
- Servier
- Allergan
- National Center for PTSD, U.S. Department of Veterans Affairs
- National Institute of Mental Health (R03MH100273, R01MH107033, R01MH087604, K23MH091254)
- Topics
- Life Sciences › Neuroscience › Biological Psychiatry › Tryptophan and brain disorders
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
- Keywords
- mood disorders, neuroinflammation, glutamate, glial cells, metabotropic glutamate receptors, ionotropic glutamate receptors, synaptic dysfunction, immune activation, glutamate clearance, synaptic loss, circuit dysfunction
- MeSH terms
- Animals, Humans, Inflammation, Synaptic Transmission, Neuroglia, Signal Transduction, Glutamic Acid, Mood Disorders
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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