Ogata T, Nakamura Y, Tsuji K, Shibata T, Kataoka K, Schubert P
Department of Physiology, Ehime University School of Medicine, Japan.
Neurosci Lett. 1994 Mar 28;170(1):5-8. doi: 10.1016/0304-3940(94)90225-9.
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.
2-氯腺苷是一种非代谢性腺苷激动剂，可增强代谢型谷氨酸激动剂（±）-1-氨基环戊烷-反式-1,3-二羧酸（t-ACPD）诱导的培养海马星形胶质细胞内钙离子浓度（[Ca2+]i）的升高。在不存在2-氯腺苷的情况下，t-ACPD的半数有效浓度（EC50）约为80微摩尔。另一方面，在存在1微摩尔2-氯腺苷的情况下，t-ACPD的EC50移至约5微摩尔，尽管最大[Ca2+]i没有变化。2-氯腺苷与t-ACPD对[Ca2+]i升高的协同作用不受细胞外钙离子消除的抑制，但受A1特异性腺苷拮抗剂的抑制。这些结果表明，腺苷可通过A1受体作为代谢型谷氨酸受体激活诱导的代谢过程的内源性共激活剂发挥作用。
