Andiné P, Orwar O, Jacobson I, Sandberg M, Hagberg H
Institute of Neurobiology, University of Göteborg, Sweden.
J Neurochem. 1991 Jul;57(1):222-9. doi: 10.1111/j.1471-4159.1991.tb02119.x.
This study addresses the possible involvement of an agonist-induced postischemic hyperactivity in the delayed neuronal death of the CA1 hippocampus in the rat. In two sets of experiments, dialytrodes were implanted into the CA1 either acutely or chronically (24 h of recovery). During 20 min of cerebral ischemia (four-vessel occlusion model) and 8 h of reflow, we followed extracellular amino acids and multiple-unit activity. Multiple-unit activity ceased within 20 sec of ischemia and remained zero during the ischemic insult and for the following 1 h of reflow. During ischemia, extracellular aspartate, glutamate, taurine, and gamma-aminobutyric acid increased in both acute and chronic experiments (seven- to 26-fold). Multiple-unit activity recovered to preischemic levels following 4-6 h of reflow. In the group with dialytrodes implanted acutely, the continuous increase in multiple-unit activity reached 110% of basal at 8 h of reflow. In the group with dialytrodes implanted chronically, multiple-unit activity recovered faster and reached 140% of control at 8 h, paralleled by an increase in extracellular aspartate (5.5-fold) and glutamate (twofold). In conclusion, the postischemic increase of excitatory amino acids and the recovery of the neuronal activity may stress the CA1 pyramidal cells, which could be detrimental in combination with, e.g., postsynaptic impairments.
本研究探讨了激动剂诱导的缺血后高活性在大鼠海马CA1区延迟性神经元死亡中可能的作用。在两组实验中，急性或慢性（恢复24小时）将透析电极植入CA1区。在20分钟的脑缺血（四动脉闭塞模型）和8小时的再灌注过程中，我们监测细胞外氨基酸和多单位活动。多单位活动在缺血20秒内停止，在缺血损伤期间以及随后1小时的再灌注过程中保持为零。在缺血期间，急性和慢性实验中细胞外天冬氨酸、谷氨酸、牛磺酸和γ-氨基丁酸均增加（7至26倍）。再灌注4至6小时后，多单位活动恢复到缺血前水平。在急性植入透析电极的组中，多单位活动持续增加，在再灌注8小时时达到基础水平的110%。在慢性植入透析电极的组中，多单位活动恢复更快，在8小时时达到对照水平的140%，同时细胞外天冬氨酸增加（5.5倍），谷氨酸增加（2倍）。总之，缺血后兴奋性氨基酸的增加和神经元活动的恢复可能会使CA1锥体细胞受到应激，这与例如突触后损伤相结合可能是有害的。
