Involvement of K(+) channels in the inhibitory effects of adenosine on anoxia-induced [Ca(2+) ](i) increase in cultured rat hippocampal CA1 neurons.

Q Wan, H Yao, F Wang
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引用次数: 8

Abstract

Changes in intracellular free Ca(2+) concentration ([Ca(2+)](i)) in cultured hippocampal CA1 neurons isolated from newborn rats were measured by a confocal laser scanning microscope, using the Ca(2+) indicator Fluo-3. The results showed that exogenous adenosine (100 microM) significantly attenuated the increase of neuronal [Ca(2+)](i) induced by acute anoxia. This effect of adenosine could be suppressed by the adenosine A1 receptor antagonist 8-cyclopentyltheophylline. Moreover, potassium channel blockers, aminopyridine, and glipizide could also block the inhibitory role of adenosine, but tetraethylammonium had no effect. These results suggest that adenosine may activate 4-AP or ATP-sensitive potassium channels via an A1-receptor-mediated mechanism and consequently inhibit anoxia-induced [Ca(2+)](i) elevation in hippocampal neurons.

K(+)通道参与腺苷对培养大鼠海马CA1神经元缺氧诱导[Ca(2+)](i)增加的抑制作用
用共聚焦激光扫描显微镜,用Ca(2+)指示剂Fluo-3测定了新生大鼠培养海马CA1神经元细胞内游离Ca(2+)浓度([Ca(2+)](i))的变化。结果表明,外源性腺苷(100 μ m)显著减弱急性缺氧诱导的神经元[Ca(2+)](i)的升高。腺苷的这种作用可被腺苷A1受体拮抗剂8-环戊基茶碱抑制。此外,钾通道阻滞剂、氨基吡啶和格列吡嗪也能阻断腺苷的抑制作用,但四乙基铵没有作用。这些结果表明腺苷可能通过a1受体介导的机制激活4-AP或atp敏感的钾通道,从而抑制缺氧诱导的海马神经元[Ca(2+)](i)升高。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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