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Endothelin-1 decreases glutamate uptake in primary cultured rat astrocytes.

Artikel i vetenskaplig tidskrift
Författare Julia Leonova
Thorleif Thorlin
N David Åberg
Peter S Eriksson
Lars Rönnbäck
Elisabeth Hansson
Publicerad i American journal of physiology. Cell physiology
Volym 281
Nummer/häfte 5
Sidor C1495-503
ISSN 0363-6143
Publiceringsår 2001
Publicerad vid Institutionen för anatomi och cellbiologi
Institutionen för klinisk neurovetenskap
Institutionen för klinisk neurovetenskap, Sektionen för laborativ neurovetenskap
Sidor C1495-503
Språk en
Länkar www.ncbi.nlm.nih.gov/entrez/query.f...
Ämnesord Amino Acid Sequence, Animals, Astrocytes, drug effects, metabolism, Barium Compounds, pharmacology, Blotting, Western, Cells, Cultured, Cerebral Cortex, cytology, drug effects, metabolism, Chlorides, pharmacology, Depression, Chemical, Endothelin-1, pharmacology, Glutamic Acid, metabolism, Immunohistochemistry, Molecular Sequence Data, Rats, Rats, Sprague-Dawley, Transduction, Genetic
Ämneskategorier Neurologi

Sammanfattning

Endothelin-1 (ET-1) is a potent vasoconstrictor peptide that is also known to induce a wide spectrum of biological responses in nonvascular tissue. In this study, we found that ET-1 (100 nM) inhibited the glutamate uptake in cultured astrocytes expressing the glutamate/aspartate transporter (GLAST); astrocytes did not express the glutamate transporter-1 (GLT-1). The V(max) and the K(m) of the glutamate uptake were reduced by 57% and 47%, respectively. Application of the ET(A) and ET(B) receptor antagonists BQ-123 and BQ-788 partly inhibited the ET-1-evoked decrease in the glutamate uptake, whereas the nonspecific ET receptor antagonist bosentan completely inhibited this decrease. Incubation of the cultures with pertussis toxin abolished the effect of ET-1 on the uptake. The ET-1-induced decrease in the glutamate uptake was independent of extracellular free Ca(2+) concentration, whereas the intracellular Ca(2+) antagonists thapsigargin and 3,4,5-trimethoxybenzoic acid 8-(diethylamino)octyl ester abolished the effect of ET-1 on the glutamate uptake. Incubation with the protein kinase C (PKC) antagonist staurosporine, but not with the fatty acid-binding protein bovine serum albumin, prevented the ET-1-induced decrease in the glutamate uptake. These results suggest that ET-1 impairs the high-affinity glutamate uptake in cultured astrocytes through a G protein-coupled mechanism, involving PKC and changes in intracellular Ca(2+).

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