Roberts E L, Sick T J
Department of Neurology, University of Miami School of Medicine, FL 33101.
Brain Res. 1988 Jul 19;456(1):113-9. doi: 10.1016/0006-8993(88)90352-6.
We examined the possibility that Ca2+-sensitive inhibition of synaptic transmission following anoxia involves compromise of ion transport activity. Rat hippocampal slices were superfused with artificial cerebrospinal fluids containing different concentrations of CaCl2, and subjected to short anoxia. Durations of anoxia were sufficient to provoke anoxic depolarization, indicated by a sudden rise in extracellular K+ (K+o). Following anoxia, apparent K+ transport was assessed by measuring the magnitude of subnormal K+o (the K+o undershoot) in hippocampal region CA1. Recovery of synaptic transmission 1 h after anoxia was determined by evaluation of the magnitudes of the orthodromically stimulated population spike recorded from CA1 pyramidal cells. K+o undershoots and recovery of synaptic transmission decreased as CaCl2 or the duration of anoxic depolarization increased. These data suggest: (1) that increased artificial cerebrospinal fluid CaCl2 compromised K+ reaccumulation after anoxia; and (2) that ion transport dysfunction may inhibit recovery of synaptic transmission.
我们研究了缺氧后Ca2+敏感的突触传递抑制涉及离子转运活性受损的可能性。用含有不同浓度CaCl2的人工脑脊液灌流大鼠海马切片，并使其经历短暂缺氧。缺氧持续时间足以引发缺氧去极化，表现为细胞外K+（K+o）突然升高。缺氧后，通过测量海马CA1区低于正常水平的K+o（K+o下冲）幅度来评估表观K+转运。通过评估从CA1锥体细胞记录的顺向刺激群体峰电位的幅度来确定缺氧1小时后突触传递的恢复情况。随着CaCl2浓度或缺氧去极化持续时间的增加，K+o下冲和突触传递的恢复减少。这些数据表明：（1）人工脑脊液中CaCl2浓度增加会损害缺氧后K+的重新积累；（2）离子转运功能障碍可能会抑制突触传递的恢复。
