Grøndahl T O, Langmoen I A
Department of Neurosurgery, Rikshospitalet, National Hospital, University of Oslo, Norway.
Neurol Res. 1996 Dec;18(6):499-504. doi: 10.1080/01616412.1996.11740461.
The increase in cytoplasmatic calcium concentration during cerebral ischemia has been proposed as a key event leading to neuronal death. In order to investigate a possible role of calcium-release from intracellular stores in ischemic neuronal injury, intracellular calcium pools were depleted prior to ischemia by the use of thapsigargin. Evoked activity (population spike) in rat hippocampal slices was monitored during a 30 min control period, 9 min of energy deprivation and 60 min of recovery. The population spike recovered to 27% (17-33) (median and 95% confidence interval) following energy deprivation in normal calcium, to 56% (50-58) in calcium-free incubation fluid and to 83% (75-88) in slices pretreated with 1 microM thapsigargin. Combining calcium removal and thapsigargin pretreatment did not improve recovery further. Both removal of extracellular calcium and emptying intracellular calcium stores prior to energy deprivation thus improved functional recovery following energy deprivation, however the latter was more effective. These results suggest that calcium release from intracellular stores may be of major importance in calcium-related neuronal injury during cerebral ischemia.
脑缺血期间细胞质钙浓度的升高被认为是导致神经元死亡的关键事件。为了研究细胞内钙库释放钙在缺血性神经元损伤中可能的作用，在缺血前使用毒胡萝卜素耗尽细胞内钙池。在30分钟的对照期、9分钟的能量剥夺期和60分钟的恢复期监测大鼠海马切片中的诱发活动（群体峰电位）。在正常钙条件下，能量剥夺后群体峰电位恢复到27%（17 - 33）（中位数和95%置信区间），在无钙孵育液中恢复到56%（50 - 58），在用1微摩尔毒胡萝卜素预处理的切片中恢复到83%（75 - 88）。联合去除钙和毒胡萝卜素预处理并未进一步改善恢复情况。因此，在能量剥夺前去除细胞外钙和排空细胞内钙库均可改善能量剥夺后的功能恢复，但后者更有效。这些结果表明，细胞内钙库释放钙在脑缺血期间与钙相关的神经元损伤中可能起主要作用。
