Phillis J W, Smith-Barbour M, Perkins L M, O'Regan M H
Department of Physiology, Wayne State University School of Medicine, Detroit, MI 48201.
Neuroreport. 1993 Jan;4(1):109-11. doi: 10.1097/00001756-199301000-00029.
The effects of the benzodiazepine derivative GYKI 52466 on ischemia-evoked neurotransmitter amino acid release were evaluated in a rat four vessel occlusion model with cerebral cortical cups. Following intravenous GYKI 52466 administration (10 mg kg-1 bolus followed by 10 mg kg-1 60 min-1 infusion) glutamate, aspartate and GABA release into cerebral cortical superfusates was enhanced by ischemia to a comparable extent to that observed in control ischemic rats. These results suggest that the protective action of GYKI 52466 against cerebral cortical ischemic injury is unlikely to be due to a selective reduction in extracellular glutamate levels, but is rather, a result of the recognized ability of this compound to block non-NMDA receptors.
在采用脑皮质杯的大鼠四血管闭塞模型中，评估了苯二氮卓衍生物GYKI 52466对缺血诱发的神经递质氨基酸释放的影响。静脉注射GYKI 52466（10mg/kg推注，随后以10mg/kg 60min-1输注）后，缺血使谷氨酸、天冬氨酸和γ-氨基丁酸释放到脑皮质灌流液中的程度与对照缺血大鼠中观察到的程度相当。这些结果表明，GYKI 52466对脑皮质缺血性损伤的保护作用不太可能是由于细胞外谷氨酸水平的选择性降低，而是该化合物阻断非NMDA受体的公认能力的结果。
