{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,7,10]],"date-time":"2026-07-10T15:11:57Z","timestamp":1783696317031,"version":"3.55.0"},"reference-count":56,"publisher":"Wiley","license":[{"start":{"date-parts":[[2014,1,1]],"date-time":"2014-01-01T00:00:00Z","timestamp":1388534400000},"content-version":"unspecified","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by\/3.0\/"}],"funder":[{"DOI":"10.13039\/100004336","name":"Novartis","doi-asserted-by":"publisher","award":["26077772"],"award-info":[{"award-number":["26077772"]}],"id":[{"id":"10.13039\/100004336","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Neural Plasticity"],"published-print":{"date-parts":[[2014]]},"abstract":"<jats:p>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<jats:sup>2+<\/jats:sup>-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<jats:sup>2+<\/jats:sup>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 E<jats:sub>2<\/jats:sub>(PGE<jats:sub>2<\/jats:sub>). Interestingly, administration of exogenous PGE<jats:sub>2<\/jats:sub>produced<jats:italic>per se<\/jats:italic>rapid, store-dependent burst exocytosis of glutamatergic vesicles in astrocytes. Finally, when PGE<jats:sub>2<\/jats:sub>-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 PGE<jats:sub>2<\/jats:sub>.<\/jats:p>","DOI":"10.1155\/2014\/254574","type":"journal-article","created":{"date-parts":[[2014,1,19]],"date-time":"2014-01-19T09:25:04Z","timestamp":1390123504000},"page":"1-11","source":"Crossref","is-referenced-by-count":25,"title":["G-Protein Coupled Receptor-Evoked Glutamate Exocytosis from Astrocytes: Role of Prostaglandins"],"prefix":"10.1155","volume":"2014","author":[{"given":"Corrado","family":"Cali","sequence":"first","affiliation":[{"name":"Department of Fundamental Neurosciences, Faculty of Biology and Medicine, University of Lausanne, rue du Bugnon 9, 1005 Lausanne, 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