Krnjević K, Xu Y Z, Zhang L
Anaesthesia Research Department, McGill University, Montréal, Québec, Canada.
Neurochem Res. 1991 Mar;16(3):279-84. doi: 10.1007/BF00966091.
In rat hippocampal slices GABAergic IPSPs are very rapidly suppressed by anoxia (in less than 2 min). Both early (GABAA) and late (GABAB) components are affected. After reoxygenation, the IPSPs recover, but only slowly and not always completely. Iontophoretic applications of GABA or baclofen indicated no major depression of responses during anoxia. It is therefore unlikely that the anoxic suppression of IPSPs is caused by desensitizations of GABA receptors. A more probable explanation is a failure of GABAergic neurons to release GABA from inhibitory nerve terminals.
在大鼠海马切片中，缺氧可非常迅速地抑制GABA能抑制性突触后电位（IPSPs）（不到2分钟）。早期（GABAA）和晚期（GABAB）成分均受到影响。复氧后，IPSPs恢复，但恢复缓慢且并非总能完全恢复。通过离子电泳施加GABA或巴氯芬表明，缺氧期间反应没有明显抑制。因此，IPSPs的缺氧抑制不太可能是由GABA受体脱敏引起的。一个更可能的解释是GABA能神经元无法从抑制性神经末梢释放GABA。
