Santucci A C, Riccio D C, Treichler F R
Department of Psychology, Kent State University, Ohio 44242.
Behav Neurosci. 1989 Dec;103(6):1267-75. doi: 10.1037//0735-7044.103.6.1267.
The present investigation assessed whether increased congruency between ACTH state present shortly after training and that at testing contributed to memory recovery. If recovery were related to an increased correspondence between internal state present after training and that at testing, then suppressing ACTH release should block memory recovery. This was the hypothesis that was examined in the present investigation. Specifically, animals were trained on a passive avoidance task, administered hypothermia (the amnestic agent) and, shortly prior to testing, given treatments known to be effective in reversing memory loss induced by hypothermia. Before training (Experiment 1) or testing (Experiment 2) animals were injected with either dexamethasone (an agent that suppresses ACTH release) or saline. Results, in general, indicated that when ACTH release was suppressed, a blunted recovery effect was obtained. This reduction in the extent of memory recovery was observed when ACTH was suppressed either at training or at testing. These data are interpreted as providing support for an ACTH-related, state-dependent retention mechanism contributing to recovery from hypothermia-induced retrograde amnesia in rats.
本研究评估了训练后不久出现的促肾上腺皮质激素（ACTH）状态与测试时的ACTH状态之间一致性的增加是否有助于记忆恢复。如果恢复与训练后出现的内部状态和测试时的内部状态之间对应性的增加有关，那么抑制ACTH释放应该会阻止记忆恢复。这就是本研究所检验的假设。具体而言，让动物接受被动回避任务训练，给予低温处理（失忆剂），并在测试前不久给予已知可有效逆转低温诱导的记忆丧失的处理。在训练前（实验1）或测试前（实验2），给动物注射地塞米松（一种抑制ACTH释放的药物）或生理盐水。总体结果表明，当ACTH释放受到抑制时，恢复效果减弱。当在训练或测试时抑制ACTH时，均观察到记忆恢复程度的降低。这些数据被解释为支持一种与ACTH相关的、状态依赖性的记忆保持机制，该机制有助于大鼠从低温诱导的逆行性遗忘中恢复。
