Laboratory of Neuropharmacology and Neural Tumor Biology, Department of Pharmacology, Institute for Basic Health Sciences, Federal University of Rio Grande do Sul, Rua Sarmento Leite, 500 (ICBS, Campus Centro/UFRGS), Porto Alegre, RS, 90050-170, Brazil.
J Neural Transm (Vienna). 2013 Nov;120(11):1525-31. doi: 10.1007/s00702-013-1032-y. Epub 2013 May 7.
Fear memory retrieval can lead to either reconsolidation (accompanied or not by strengthening of the memory trace) or extinction. Here, we show that non-reinforced retrieval of inhibitory avoidance (IA) conditioning can induce memory strengthening assessed in a subsequent retention test trial. Infusion of the protein synthesis inhibitor cycloheximide or the mTOR inhibitor rapamycin into the rat basolateral complex of the amygdala (BLA) after a reactivation (retrieval) session impaired retrieval-induced strengthening. Intra-BLA infusion of the mRNA synthesis inhibitor 5,6-dichloro-1-beta-D-ribofuranosylbenzimidazole (DRB) after retrieval had no effect. These findings provide the first evidence suggesting that non-reinforced IA retrieval can lead to memory strengthening through a mechanism dependent on protein synthesis and mTOR activity in the BLA.
恐惧记忆的提取会导致再巩固（伴随或不伴随记忆痕迹的增强）或遗忘。在这里，我们表明，非强化的抑制性回避（IA）条件反射的提取可以在随后的保留测试中诱导记忆增强。在重新激活（检索）后，将蛋白质合成抑制剂环己亚胺或 mTOR 抑制剂雷帕霉素注入大鼠杏仁核基底外侧复合体（BLA）中，会损害检索诱导的增强。提取后 BLA 内注射 mRNA 合成抑制剂 5,6-二氯-1-β-D-核糖呋喃基苯并咪唑（DRB）没有影响。这些发现提供了第一个证据，表明非强化的 IA 检索可以通过依赖于 BLA 中的蛋白质合成和 mTOR 活性的机制导致记忆增强。
