ArticleNeural plasticity2014
G-protein coupled receptor-evoked glutamate exocytosis from astrocytes: role of prostaglandins.
Article in Neural plasticity, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 28 citations in OpenAlex.
- Involvement of COX-2 in the Neurovascular Unit Damage Through Up-Regulating Calpain/PARP/NF-κB Inflammatory Signaling During Ischemic Stroke.Neurochemical research · 2026Article
- Astrocyte Dysfunctions in Obsessive Compulsive Disorder: Rethinking Neurobiology and Therapeutic Targets.Journal of neurochemistry · 2025Review
- Metabolic Reprogramming of Astrocytes in Pathological Conditions: Implications for Neurodegenerative Diseases.International journal of molecular sciences · 2024Review
- Brain oxidative stress mediates anxiety-like behavior induced by indomethacin in zebrafish: protective effect of alpha-tocopherol.Naunyn-Schmiedeberg's archives of pharmacology · 2024Article
- Metabolic dynamics in astrocytes and microglia during post-natal development and their implications for autism spectrum disorders.Frontiers in cellular neuroscience · 2024Review
- Regulated exocytosis from astrocytes: a matter of vesicles?Frontiers in neuroscience · 2024Article
- Review
- Review
- Receptor mechanisms underlying the CNS effects of cannabinoids: CBAdvances in pharmacology (San Diego, Calif.) · 2022Article
- The Strategic Location of Glycogen and Lactate: From Body Energy Reserve to Brain Plasticity.Frontiers in cellular neuroscience · 2019Article
- A computational study of astrocytic glutamate influence on post-synaptic neuronal excitability.PLoS computational biology · 2018Article
- Olig2-Lineage Astrocytes: A Distinct Subtype of Astrocytes That Differs from GFAP Astrocytes.Frontiers in neuroanatomy · 2018Article
- Homer1 Scaffold Proteins Govern Ca2+ Dynamics in Normal and Reactive Astrocytes.Cerebral cortex (New York, N.Y. : 1991) · 2017Article
- Crosstalk Among Disrupted Glutamatergic and Cholinergic Homeostasis and Inflammatory Response in Mechanisms Elicited by Proline in Astrocytes.Molecular neurobiology · 2016Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Astrocytes are highly secretory cells, participating in rapid brain communication by releasing glutamate. Recent evidences have suggested that this process is largely mediated by Ca(2+)-dependent regulated exocytosis of VGLUT-positive vesicles. Here by taking advantage of VGLUT1-pHluorin and TIRF illumination, we characterized mechanisms of glutamate exocytosis evoked by endogenous transmitters (glutamate and ATP), which are known to stimulate Ca(2+) elevations in astrocytes. At first we characterized the VGLUT1-pHluorin expressing vesicles and found that VGLUT1-positive vesicles were a specific population of small synaptic-like microvesicles containing glutamate but which do not express VGLUT2. Endogenous mediators evoked a burst of exocytosis through activation of G-protein coupled receptors. Subsequent glutamate exocytosis was reduced by about 80% upon pharmacological blockade of the prostaglandin-forming enzyme, cyclooxygenase. On the other hand, receptor stimulation was accompanied by extracellular release of prostaglandin E2 (PGE2). Interestingly, administration of exogenous PGE2 produced per se rapid, store-dependent burst exocytosis of glutamatergic vesicles in astrocytes. Finally, when PGE2-neutralizing antibody was added to cell medium, transmitter-evoked exocytosis was again significantly reduced (by about 50%). Overall these data indicate that cyclooxygenase products are responsible for a major component of glutamate exocytosis in astrocytes and that large part of such component is sustained by autocrine/paracrine action of PGE2.
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