Shan H Q, Cheng J S
National Laboratory of Medical Neurobiology, Department of Neurobiology, Shanghai Medical University, 138 YiXueYuan Road, 200032, People's Republic of, Shanghai, China.
Neurosci Lett. 2000 May 26;286(1):45-8. doi: 10.1016/s0304-3940(00)01083-1.
Using the whole-cell patch clamp method, we explored the effect of adenosine on the K(ATP) current and its regulatory mechanisms in acutely dissociated rat hippocampal neurons. A chemical hypoxia model was made using 0.2 mmol/l 2,4dinitrophenol (2,4DNP). During hypoxia, the K(ATP) current was not raised significantly by adenosine alone, but was accelerated significantly by adenosine in combination with the selective A(2) receptor blocker 3, 7-dimethl-1-propargylxanth-ine. The selective A(1) receptor agonist N6-cyclopentyladenosine also accelerated the K(ATP) current. These results suggest that activation of the adenosine A(1) receptor can accelerate opening of the K(ATP) channel during hypoxia, and that the A(2) receptor may have an opposing effect to the A(1) receptor.
采用全细胞膜片钳技术，我们探讨了腺苷对急性分离的大鼠海马神经元中K(ATP)电流的影响及其调控机制。使用0.2 mmol/l 2,4-二硝基苯酚（2,4-DNP）建立化学性缺氧模型。在缺氧期间，单独使用腺苷时K(ATP)电流未显著升高，但腺苷与选择性A(2)受体阻滞剂3,7-二甲基-1-丙炔基黄嘌呤联合使用时，K(ATP)电流显著加快。选择性A(1)受体激动剂N6-环戊基腺苷也能加快K(ATP)电流。这些结果表明，缺氧时腺苷A(1)受体的激活可加速K(ATP)通道的开放，且A(2)受体可能对A(1)受体具有相反的作用。
