Neuroligand‐Evoked Calcium‐Dependent Release of Excitatory Amino Acids from Cultured Astrocytes
Neuroligand‐Evoked Calcium‐Dependent Release of Excitatory Amino Acids from Cultured Astrocytes
复制标题
神经配体诱发培养星形胶质细胞钙依赖性兴奋性氨基酸的释放
作者:
S. Jeftinija;K. Jeftinija;G. Stefanović;Fang Liu
Abstract: 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.
DOI:
10.1073/pnas.87.9.3454
发表时间:
1990-05-01
影响因子:
11.1
作者:
GLAUM, SR;HOLZWARTH, JA;MILLER, RJ
通讯作者:
MILLER, RJ
影响因子:
2.9
作者:
Blau,L;Weissmann,G
通讯作者:
Weissmann,G
影响因子:
56.9
作者:
CORNELLBELL, AH;FINKBEINER, SM;SMITH, SJ
通讯作者:
SMITH, SJ