Calcium signaling and gliotransmission in normal vs. reactive astrocytes
Open accessAbstract
A prominent area of neuroscience research over the past 20 years has been the acute modulation of neuronal synaptic activity by Ca(2+)-dependent release of the transmitters ATP, D-serine, and glutamate (called gliotransmitters) by astrocytes. Although the physiological relevance of this mechanism is under debate, emerging evidence suggests that there are critical factors in addition to Ca(2+) that are required for gliotransmitters to be released from astrocytes. Interestingly, these factors include activated microglia and the proinflammatory cytokine Tumor Necrosis Factor α (TNFα), chemotactic cytokine Stromal cell-Derived Factor-1α (SDF-1α), and inflammatory mediator prostaglandin E2 (PGE(2)). Of note, microglial activation and release of inflammatory molecules from activated microglia and reactive astrocytes can occur within minutes of a triggering stimulus. Therefore, activation of astrocytes by inflammatory molecules combined with Ca(2+) elevations may lead to gliotransmitter release, and be an important step in the early sequence of events contributing to hyperexcitability, excitotoxicity, and neurodegeneration in the damaged or diseased brain. In this review, we will first examine evidence questioning Ca(2+)-dependent gliotransmitter release from astrocytes in healthy brain tissue, followed by a close examination of recent work suggesting that Ca(2+)-dependent gliotransmitter release occurs as an early event in the development of neurological disorders and neuroinflammatory and neurodegenerative diseases.
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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 Agulhon et al., 2012
The section on activated microglia and reactive astrocytes describes inflammatory mediators producing astrocytic Ca2+ elevations and glutamate release; the Summary and Perspectives likewise links reactive astrocytes to Ca2+-dependent glutamate release. These passages support the calcium-signaling part, but concern glutamate release, not an effect of immune activation on cellular glutamate uptake. No page number is provided in our copy. (LLM, conf=0.86)
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- Authors
- Agulhon, C., Sun, M.-Y., Murphy, T., Myers, T., Lauderdale, K., & Fiacco, T. A.
- Affiliations
- Centre National de la Recherche Scientifique (FR)
- University of California, Riverside (US)
- Corresponding author
- Agulhon, Cendra
- Venue
- Frontiers in Pharmacology
- Publisher
- Frontiers Media SA
- Published
- 2012
- Volume
- 3
- Pages
- 139-139
- ISSN
- 1663-9812 (ISSN-L)
- PMC
- PMC3395812
- OpenAlex
- W1965276722
- Cited by
- 167
- References
- 167
- Citations by year
- 2026: 5 · 2025: 12 · 2024: 10 · 2023: 14 · 2022: 8 · 2021: 16 · 2020: 11 · 2019: 9 · 2018: 13 · 2017: 9 · 2016: 14 · 2015: 17 · 2014: 16 · 2013: 10 · 2012: 2
- FWCI
- 5.93
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- cc-by
- Locations
- Frontiers in Pharmacology (publishedVersion, cc-by)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Funders
- Hellman Foundation
- Topics
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Physiology › Adenosine and Purinergic Signaling
- Keywords
- calcium signaling, gliotransmission, reactive astrocytes, ATP release, D-serine, glutamate release, microglial activation, TNF-α, stromal cell-derived factor-1α, prostaglandin E2, neuroinflammation, neurodegeneration, excitotoxicity, hyperexcitability
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