Zini S, Roisin M P, Armengaud C, Ben-Ari Y
Laboratoire de Neurobiologie et Physiopathologie du Développement, INSERM U29, Paris, France.
Neurosci Lett. 1993 Apr 30;153(2):202-5. doi: 10.1016/0304-3940(93)90322-c.
The effects of the potassium channel openers lemakalim, RP 52891 and galanin and the potassium channel blockers glibenclamide and gliquidone were evaluated by the release of endogenous glutamate from rat hippocampal slices subjected to a brief period of ischaemia (2-10 min). Ischaemia was mimicked by incubating slices in a glucose free medium equilibrated with 95% N2/5% CO2. These conditions evoked a release of glutamate which was insensitive to tetrodotoxin and Ca2+ indicating a non-vesicular origin. The release of glutamate evoked by a 6- or 8-min period of ischaemia was reduced by 25-40% in the presence of lemakalim (10 microM), RP 52891 (10 microM) or galanin (0.3 microM), whereas it was enhanced by 60 to 100% in the presence of glibenclamide (1 microM) and gliquidone (2 microM). These observations suggest that cellular damage resulting from ischaemia induced excessive release of glutamate in the hippocampus may be partly reduced by potassium channel openers, and conversely increased by sulfonylureas.
通过短暂缺血（2 - 10分钟）的大鼠海马切片释放内源性谷氨酸，评估钾通道开放剂乐卡地平、RP 52891和甘丙肽以及钾通道阻滞剂格列本脲和格列喹酮的作用。通过在与95% N2/5% CO2平衡的无葡萄糖培养基中孵育切片来模拟缺血。这些条件引起的谷氨酸释放对河豚毒素和Ca2+不敏感，表明其非囊泡来源。在乐卡地平（10 microM）、RP 52891（10 microM）或甘丙肽（0.3 microM）存在的情况下，6或8分钟缺血引起的谷氨酸释放减少了25 - 40%，而在格列本脲（1 microM）和格列喹酮（2 microM）存在的情况下，谷氨酸释放增加了60%至100%。这些观察结果表明，缺血诱导的海马中谷氨酸过度释放所导致的细胞损伤可能部分被钾通道开放剂减少，相反地，被磺脲类药物增加。
