Paolino R M, Levy H M
Science. 1971 May 14;172(3984):746-9. doi: 10.1126/science.172.3984.746.
Rats were given electroconvulsive shock and bilateral cortical spreading depression, either alone or in combination, at various times after a single passive avoidance training trial. Assessment of retention deficits, 24 hours after training, revealed a U-shaped amnesic function for cortical spreading depression as compared with the short linear function consistently obtained with electroconvulsive shock in this situation. Induction of cortical spreading depression immediately after training resulted in an extension of the amnesic gradient produced by electroconvulsive shock, presumably by disruption of the subcortically confined memory trace. In addition to indicating a stibcortical locus of action for the amnesic effects of electroconvulsive shock, these results are interpreted as favoring a hypothesis of time-dependent memory trace localization in short-term memory processing, which involves an initial subcortical localization of the trace followed by a phase involving either direct or indlirect cortical participation in a mulltistage memory fixation process.
在单次被动回避训练试验后的不同时间，对大鼠单独或联合给予电惊厥休克和双侧皮质扩散性抑制。训练24小时后对记忆缺陷的评估显示，与在这种情况下电惊厥休克一贯产生的短线性遗忘功能相比，皮质扩散性抑制呈现出U形遗忘功能。训练后立即诱发皮质扩散性抑制导致电惊厥休克产生的遗忘梯度延长，这可能是由于破坏了皮质下局限的记忆痕迹。这些结果除了表明电惊厥休克遗忘效应的皮质下作用位点外，还被解释为支持短期记忆加工中时间依赖性记忆痕迹定位的假说，该假说涉及记忆痕迹最初在皮质下的定位，随后是一个阶段，在这个多阶段记忆巩固过程中，涉及直接或间接的皮质参与。
