Wan Q, Wang F Z, Yao H, Liu Z W, Huang Y H, Ding A S
Institute of Basic Medical Sciences, Beijing.
Sheng Li Xue Bao. 1997 Oct;49(5):545-50.
Intracellular free Ca2+ concentration ([Ca2+]i) was measured by laser scanning confocal microscope, using Ca2+ indicator Fluo-3 in cultured hippocampal CA1 neurons isolated from newborn rat. The results showed that acute anoxia induced a rapid increase of [Ca2+]i in hippocampal CA1 neurons, and this increase could be attenuated by 100 mumol/L adenosine significantly. This effect of adenosine could be suppressed by adenosine A1 receptor antagonist CPT or potassium channel blockers, 4-AP and glipizide. These results suggest that adenosine activates 4-AP- or ATP-sensitive potassium channels through A1 receptors, and consequently inhibits the [Ca2+]i elevation in hippocampal neurons during anoxia.
使用从新生大鼠分离的培养海马CA1神经元中的Ca2+指示剂Fluo-3，通过激光扫描共聚焦显微镜测量细胞内游离Ca2+浓度（[Ca2+]i）。结果表明，急性缺氧诱导海马CA1神经元中[Ca2+]i迅速增加，而100μmol/L腺苷可显著减弱这种增加。腺苷的这种作用可被腺苷A1受体拮抗剂CPT或钾通道阻滞剂4-AP和格列吡嗪抑制。这些结果表明，腺苷通过A1受体激活4-AP或ATP敏感性钾通道，从而在缺氧期间抑制海马神经元中[Ca2+]i的升高。
