Department of Anesthesiology, First Affiliated Hospital of ChongQing Medical University, ChongQing, China.
J ECT. 2010 Jun;26(2):126-30. doi: 10.1097/yct.0b013e3181a9947a.
This animal study tested the spatial learning memory of "depressed" rats undergoing electroconvulsive therapy (ECT) or ECT combined with propofol and aimed to reveal the glutamatergic mechanisms in the hippocampus.
Sixty Sprague-Dawley rats were randomly divided into 5 groups (n = 12 rats per group): control group, depression group, propofol group, ECT group, and propofol + ECT group. Rats were stressed repeatedly for 21 days to establish depression model. After the model was set up, rats of the propofol group were administrated with propofol (100 mg/kg). Rats of ECT group were administered ECT once on alternate days for 2 weeks. ECT + propofol group rats were given ECT after anesthesia with propofol (100 mg/kg). Spatial memory was assessed by Morris water maze. Glutamate content in hippocampus was measured by chromatometry. N-methyl d-aspartate (NMDA)-NR2B expression was detected by immunohistochemistry.
After treatment, the behavior level of rats in ECT group and ECT + propofol group was higher than that in depression group, and there was no significance between ECT group and ECT + propofol group. The evasive latency of rats detected by Morris water maze got shorter and shorter from the first day to fourth day. The evasive latency in ECT group was longer than that in ECT + propofol group and depression group, and the evasive latency in ECT + propofol group was shorter than that in depression group. Glutamate contents in hippocampus of rats in depression group and propofol group were higher than those in other groups, and glutamate content in ECT group was lower than that in other groups. The content in ECT + propofol group was lower than that in depression group, but higher than that in ECT group. N-methyl d-aspartate-NR2B expression in hippocampus of rats in depression group was lower than that in control group, but the expressions in ECT group and ECT + propofol group were higher than that in control group, and the expression in ECT + propofol group was lower than that in ECT group.
The glutamate content in hippocampus of depressed rats heightens, and the NMDA-NR2B expression down-regulated, which may cause "depression" symptoms and learning memory impairment. After ECT, the glutamate contents decreased, and NMDA-NR2B expression up-regulated, the depression symptoms improved, and the spatial memory worsened simultaneously. However, propofol inhibited the excessive decrease of glutamate and excessive up-regulation of NMDA-NR2B caused by ECT, and both the depression symptoms and the spatial memory of depressed rats improved.
本动物研究测试了接受电惊厥疗法（ECT）或 ECT 联合异丙酚治疗的“抑郁”大鼠的空间学习记忆，旨在揭示海马中的谷氨酸能机制。
将 60 只 Sprague-Dawley 大鼠随机分为 5 组（每组 12 只大鼠）：对照组、抑郁组、异丙酚组、ECT 组和异丙酚+ECT 组。大鼠反复应激 21 天以建立抑郁模型。建立模型后，异丙酚组大鼠给予异丙酚（100mg/kg）。ECT 组大鼠每两天给予 ECT 一次，共 2 周。ECT+异丙酚组大鼠在异丙酚（100mg/kg）麻醉后给予 ECT。通过 Morris 水迷宫评估空间记忆。通过色谱法测量海马中的谷氨酸含量。通过免疫组织化学检测 N-甲基-D-天冬氨酸（NMDA）-NR2B 表达。
治疗后，ECT 组和 ECT+异丙酚组大鼠的行为水平高于抑郁组，ECT 组与 ECT+异丙酚组之间无显著性差异。大鼠通过 Morris 水迷宫检测到的逃避潜伏期从第一天到第四天逐渐缩短。ECT 组的逃避潜伏期长于 ECT+异丙酚组和抑郁组，而 ECT+异丙酚组的逃避潜伏期短于抑郁组。抑郁组和异丙酚组大鼠海马中的谷氨酸含量高于其他组，而 ECT 组的谷氨酸含量低于其他组。ECT+异丙酚组的含量低于抑郁组，但高于 ECT 组。抑郁组大鼠海马中 N-甲基-D-天冬氨酸-NR2B 表达低于对照组，但 ECT 组和 ECT+异丙酚组的表达高于对照组，而 ECT+异丙酚组的表达低于 ECT 组。
抑郁大鼠海马中的谷氨酸含量升高，NMDA-NR2B 表达下调，可能导致“抑郁”症状和学习记忆障碍。ECT 后，谷氨酸含量降低，NMDA-NR2B 表达上调，抑郁症状改善，同时空间记忆恶化。然而，异丙酚抑制了 ECT 引起的谷氨酸过度减少和 NMDA-NR2B 过度上调，改善了抑郁大鼠的抑郁症状和空间记忆。
