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本实验采用海马脑片细胞外记录技术，观察了缺氧早期突触功能可逆性抑制中腺苷的作用并初步探讨其作用机制。结果发现：海马脑片缺氧早期突触功能出现可逆性抑制，与外源施加高浓度腺苷反应类同。腺苷Ａ１受体拮抗剂ＣＰＴ以及Ｋ＋通道阻断剂４－ＡＰ可阻断这种抑制作用；而ＴＥＡ以及ＡＴＰ敏感Ｋ＋通道阻断剂ｇｌｉｐｉｚｉｄｅ均未见显著效应。结果提示：缺氧早期突触功能可逆性抑制与内源性腺苷大量释放有关，腺苷通过作用其Ａ１受体，激活４－ＡＰ敏感Ｋ＋通道，从而抑制突触传递，显示其抗缺氧作用。ＡＴＰ敏感性Ｋ＋通道可能不参于这个过程。
In this study, we used hippocampal slice extracellular recording technology to observe the reversible inhibition of adenosine by early synaptic function in hypoxia and to explore its mechanism. The results showed that hippocampal slices had reversible inhibition of synaptic function in early hypoxia, which was similar to the exogenous application of adenosine at high concentrations. Adenosine A1 receptor antagonist CPT and K + channel blocker 4-AP can block this inhibition; TEA and ATP-sensitive K + channel blocker glipizide showed no significant effect. The results suggest that the reversible inhibition of synaptic function in early hypoxia is related to the release of large quantities of endogenous adenosine, which inhibits synaptic transmission by activating its A1 receptor and activating 4-AP-sensitive K + channels, demonstrating its anti-hypoxic effects . ATP-sensitive K + channels may not participate in this process.