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Neuroligand‐Evoked Calcium‐Dependent Release of Excitatory Amino Acids from Cultured Astrocytes
Author(s) -
Jeftinija Srdija D.,
Jeftinija Ksenija V.,
Stefanovic Gordana,
Liu Fang
Publication year - 1996
Publication title -
journal of neurochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.75
H-Index - 229
eISSN - 1471-4159
pISSN - 0022-3042
DOI - 10.1046/j.1471-4159.1996.66020676.x
Subject(s) - glutamate receptor , calcium , exocytosis , astrocyte , excitotoxicity , neurotransmitter , biology , ionomycin , biochemistry , glutamic acid , neurotoxin , stimulation , chemistry , biophysics , endocrinology , amino acid , receptor , central nervous system , organic chemistry , secretion
The release of excitatory amino acids (EAAs) from neuron‐free cultures of neocortical astrocytes was monitored using HPLC. The neuroligand bradykinin caused a dose‐dependent receptor‐mediated increase in release of the EAAs glutamate and aspartate from type 1 astrocyte cell cultures obtained from rat cerebral cortex. Removal of calcium from the extracellular fluid prevented the bradykinin‐induced release of EAAs from astrocytes. The addition of the calcium ionophore ionomycin caused a calcium‐dependent release of EAAs. Inhibitors of the glutamate transporters p ‐chloromercuriphenylsulfonic acid, l ‐ trans ‐pyrrolidine‐2,4‐dicarboxylate, and dihydrokainate failed to impair the ability of bradykinin to stimulate glutamate release from astrocytes. α‐Latrotoxin, an active compound of black widow spider venom, caused a significant increase of the release of glutamate in calcium‐containing saline. In calcium‐depleted saline, α‐latrotoxin produced an initial increase in the concentration of glutamate followed by a decline in the concentration of glutamate indicating stimulation of exocytosis coupled with low calcium‐induced inhibition of endocytosis. Taken together, these data suggest that astrocytes may release neurotransmitter through a mechanism that is similar to the neuronal secretory process. Given the important role of glutamate in the induction of long‐term potentiation, learning, memory, and excitotoxicity, it will be important to determine external signals that control both the uptake and release of glutamate by astrocytes.