Wan Q, Wang F, Liu Z, Kuang P, Wu W
Institute of Basic Medical Sciences, Beijing.
Zhongguo Ying Yong Sheng Li Xue Za Zhi. 1997 May;13(2):102-5.
The role of adenosine in reversible inhibition of synaptic function during the early stage of anoxia and its mechanisms were investigated with extracellular recording technique in rat hippocampal slices. The results showed that acute anoxia led to the reversible inhibition of synaptic function, which is similar to the response to addition of high concentration of exogenous adenosine. The reversible inhibition could be suppressed by adenosine A1 receptor antagonist CPT and potassium channel blocker 4-AP, whereas TEA and ATP-sensitive potassium channel blocker glipzide had no effect. These results suggest that during the early stage of anoxia, the enhanced release of endogenous adenosine can inhibit the synaptic transmission by activating 4-AP-sensitive potassium channels via A1 receptors and thus play a role in protenction against anoxic injury. ATP-sensitive potassium channels may not be involved in the mechanisms of adenosine action.
采用细胞外记录技术，在大鼠海马脑片中研究了腺苷在缺氧早期对突触功能的可逆性抑制作用及其机制。结果表明，急性缺氧导致突触功能的可逆性抑制，这与添加高浓度外源性腺苷后的反应相似。腺苷A1受体拮抗剂CPT和钾通道阻滞剂4-AP可抑制这种可逆性抑制，而TEA和ATP敏感性钾通道阻滞剂格列本脲则无作用。这些结果提示，在缺氧早期，内源性腺苷释放增加可通过A1受体激活4-AP敏感性钾通道，从而抑制突触传递，在缺氧性损伤的保护中发挥作用。ATP敏感性钾通道可能不参与腺苷作用的机制。
