<i>α</i>‐Latrotoxin stimulates glutamate release from cortical astrocytes in cell culture
FEBS LettersPublished 6 March 1995Open access
V Parpura, F Liu, S Brethorst, K. Jeftinija, S. Jeftinija, Philip G. Haydon
Citations79
SJR quartileQ1
SJR score1.22
SNIP0.77
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TL;DR
The mechanism responsible for the ability of bradykinin to cause calcium‐dependent release of glutamate from astrocytes in vitro was investigated and α‐latrotoxin, a component of black widow spider venom, stimulated calcium‐independent glutamate release from ast rocytes, suggesting that astroCytes may release neurotransmitter using a mechanism similar to the neuronal secretory process.
Abstract
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. alpha-Latrotoxin (3 nM), a component of black widow spider venom, stimulated calcium-independent glutamate release from astrocytes. Since alpha-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.
Keywords
Biochemistry, Genetics and Molecular Biology
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