G-protein coupled receptor-evoked glutamate exocytosis from astrocytes: role of prostaglandins.

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Serval ID
serval:BIB_557592B10C9C
Type
Article: article from journal or magazin.
Collection
Publications
Institution
Title
G-protein coupled receptor-evoked glutamate exocytosis from astrocytes: role of prostaglandins.
Journal
Neural Plasticity
Author(s)
Cali C., Lopatar J., Petrelli F., Pucci L., Bezzi P.
ISSN
1687-5443 (Electronic)
Publication state
Published
Issued date
2014
Volume
2014
Pages
254574
Language
english
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.
Pubmed
Web of science
Open Access
Yes
Create date
21/02/2014 18:18
Last modification date
20/08/2019 14:10
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