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α ‐Latrotoxin stimulates glutamate release from cortical astrocytes in cell culture
Author(s) -
Vladimir Parpura,
Fang Liu,
Susan Brethorst,
Ksenija Jeftinija,
Srdija Jeftinija,
Philip G. Haydon
Publication year - 1995
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/0014-5793(95)00121-o
Subject(s) - glutamate receptor , bradykinin , neurotransmitter , astrocyte , calcium , chemistry , exocytosis , neuroglia , biology , biochemistry , microbiology and biotechnology , biophysics , neuroscience , central nervous system , membrane , receptor , organic chemistry
The mechanism responsible for the ability of bradykinin to cause calcium‐dependent release of glutamate from astrocytes in vitro was investigated. The glutamate transport inhibitor, dihydrokainate, did not block bradykinin‐induced glutamate release, and bradykinin did not cause cell swelling. These data exclude the involvement of glutamate transporters or swelling mechanisms as mediating glutamate release in response to bradykinin. α ‐Latrotoxin (3 nM), a component of black widow spider venom, stimulated calcium‐independent glutamate release from astrocytes. Since α ‐latrotoxin induces vesicle fusion and calcium‐independent neuronal neurotransmitter release, our data suggest that astrocytes may release neurotransmitter using a mechanism similar to the neuronal secretory process.