Bohbot V, Otáhal P, Liu Z, Nadel L, Bures J
Arizona Research Laboratories, Neural Systems Memory and Aging, University of Arizona, Tucson 85721, USA.
Proc Natl Acad Sci U S A. 1996 Apr 30;93(9):4016-9. doi: 10.1073/pnas.93.9.4016.
Head trauma leading to concussion and electroconvulsive shock (ECS) in humans causes amnesia for events that occurred shortly before the injury (retrograde amnesia). The present experiment investigated the amnesic effect of lidocaine and ECS in 25 rats trained on a working memory version of the Morris water task. Each day, the escape platform was moved to a new location; learning was evidenced by a decrease in the latency to find the platform from the first to the second trial. "Consolidation" of this newly encoded spatial engram was disrupted by bilateral inactivation of the dorsal hippocampus with 1 microliter of 4% lidocaine applied as soon as possible after the first trial. When trial 2 was given after recovery from the lidocaine (30 min after the injection), a normal decrease in latency indicated that the new engram was not disrupted. When trial 2 was given under the influence of lidocaine (5 min after injection), absence of latency decrease demonstrated both the success of the inactivation and the importance of hippocampus for the task. To examine the role of events immediately after learning, ECS (30 or 100 mA, 50 Hz, 1.2 sec) was applied 0 sec to 45 sec after a single escape to the new platform location. A 2-h delay between ECS and trial 2 allowed the effects of ECS to dissipate. ECS applied 45 sec or 30 sec after trial 1 caused no retrograde amnesia: escape latencies on trial 2 were the same as in control rats. However, ECS applied 0 sec or 15 sec after trial 1 induced clear retrograde amnesia: escape latencies on trial 2 were no shorter than on trial 1. It is concluded that the consolidation of a newly formed memory for spatial location can only be disrupted by ECS within 30 sec after learning.
头部创伤导致人类脑震荡和电惊厥休克（ECS）会造成对受伤前不久发生的事件失忆（逆行性失忆）。本实验研究了利多卡因和ECS对25只在莫里斯水迷宫工作记忆版本任务中接受训练的大鼠的失忆作用。每天，逃生平台会被移到一个新位置；从第一次试验到第二次试验找到平台的潜伏期缩短证明了学习的发生。在第一次试验后尽快向双侧背侧海马注射1微升4%利多卡因使其失活，会破坏这种新编码的空间记忆痕迹的“巩固”。当在利多卡因作用消失后（注射后30分钟）进行第二次试验时，潜伏期正常缩短表明新的记忆痕迹未被破坏。当在利多卡因作用下（注射后5分钟）进行第二次试验时，潜伏期没有缩短既证明了失活的成功，也证明了海马体对该任务的重要性。为了研究学习后即刻事件的作用，在单次逃向新平台位置后0秒至45秒施加ECS（30或100毫安，50赫兹，1.2秒）。在ECS和第二次试验之间延迟2小时，以使ECS的作用消散。在试验1后45秒或30秒施加ECS不会导致逆行性失忆：第二次试验的逃生潜伏期与对照大鼠相同。然而，在试验1后0秒或15秒施加ECS会引发明显的逆行性失忆：第二次试验的逃生潜伏期不短于第一次试验。得出的结论是，新形成的空间位置记忆的巩固只能在学习后30秒内被ECS破坏。
