Adenosine enhances intracellular Ca2+ mobilization in conjunction with metabotropic glutamate receptor activation by t-ACPD in cultured hippocampal astrocytes.
2Cl-Adenosine, a non-metabolized adenosine agonist, enhanced the increase in intracellular Ca2+ concentration ([Ca2+]i) in cultured hippocampal astrocytes induced by (+-)-1-aminocyclopentane-trans-1,3-dicarboxylic acid (t-ACPD), a metabotropic glutamate agonist. In the absence of 2Cl-adenosine, the half effective concentration (EC50) of t-ACPD was about 80 microM. On the other hand, in the presence of 1 microM 2Cl-adenosine, the EC50 of t-ACPD shifted to about 5 microM, although the maximum [Ca2+]i did not change. The synergistic effect of 2Cl-adenosine with t-ACPD on [Ca2+]i elevation was not inhibited by the elimination of extracellular Ca2+, but was inhibited by A1-specific adenosine antagonists. These results indicate that adenosine can act via the A1 receptor as an endogenous co-activator of the metabolic processes induced by metabotropic glutamate receptor activation.
Ogata
T
T
Department of Physiology, Ehime University School of Medicine, Japan.
Nakamura
Y
Y
Tsuji
K
K
Shibata
T
T
Kataoka
K
K
Schubert
P
P
D000241:Adenosine / Q000494:pharmacology*; D000818:Animals; D001253:Astrocytes / Q000187:drug effects / Q000378:metabolism*; D002118:Calcium / Q000378:metabolism*; D002478:Cells, Cultured; D003515:Cycloleucine / Q000031:analogs & derivatives* / Q000494:pharmacology; D004357:Drug Synergism; D006624:Hippocampus / Q000166:cytology / Q000187:drug effects / Q000378:metabolism*; D009498:Neurotoxins / Q000494:pharmacology*; D058915:Purinergic P1 Receptor Antagonists; D051381:Rats; D018094:Receptors, Metabotropic Glutamate / Q000187:drug effects / Q000378:metabolism*
D009498:Neurotoxins; D058915:Purinergic P1 Receptor Antagonists; D018094:Receptors, Metabotropic Glutamate; D003515:Cycloleucine; C036361:1-amino-1,3-dicarboxycyclopentane; D000241:Adenosine; D002118:Calcium