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Glutamate release from astrocytes is stimulated via the appearance of exocytosis during cyclic AMP‐induced morphologic changes
Author(s) -
Shiga Hatsuki,
Murakami Jun,
Nagao Takashi,
Tanaka Motoki,
Kawahara Koichi,
Matsuoka Ichiro,
Ito Etsuro
Publication year - 2006
Publication title -
journal of neuroscience research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.72
H-Index - 160
eISSN - 1097-4547
pISSN - 0360-4012
DOI - 10.1002/jnr.20885
Subject(s) - exocytosis , glutamate receptor , astrocyte , microbiology and biotechnology , neuroglia , biology , stimulation , neurotransmission , extracellular , synaptic vesicle , glutamic acid , chemistry , biochemistry , neuroscience , vesicle , membrane , receptor , central nervous system , amino acid
Recent studies have shown that astrocytes release various transmitters including glutamate and thus directly affect synaptic neurotransmission. The mechanisms involved in the release of glutamate from astrocytes remain unclear, however. In the present study, we examined differences in 1) the amount of glutamate released, 2) the appearance of exocytosis, and 3) the expression of SNARE (soluble N ‐ethylmaleimide sensitive fusion protein attachment protein receptor) proteins between cyclic AMP‐treated and non‐treated astrocytes in culture. Extracellular glutamate was detected in the recording solution of cyclic AMP‐treated astrocytes after stimulation with ATP by high‐performance liquid chromatography and NADH imaging. Exocytosis, which was observed by FM1‐43 imaging, appeared in cyclic AMP‐treated astrocytes in a punctiform fashion, but not in non‐treated cells, after stimulation with ATP and glutamate. Immunocytochemistry and Western blotting showed that the amount of SNARE proteins increased during cAMP‐induced morphologic changes, and in particular, a v‐SNARE, synaptobrevin, appeared as punctiform staining in the cytosol of cyclic AMP‐treated astrocytes. These findings show that astrocytes acquire SNARE proteins during cyclic AMP‐induced differentiation, and suggest that glutamate is released by exocytosis in cyclic AMP‐treated astrocytes in response to ATP released from neighboring neurons and astrocytes. © 2006 Wiley‐Liss, Inc.