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Anisomycin infused into the hippocampus fails to block reconsolidation but impairs extinction: The role of re-exposure duration

机译:注入海马的茴香霉素不能阻止再巩固但会损害灭绝:再暴露持续时间的作用

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摘要

Recent studies have reported new evidence consistent with the hypothesis that reactivating a memory by re-exposure to a training context destabilizes the memory and induces “reconsolidation.” In the present experiments, rats' memory for inhibitory avoidance (IA) training was tested 6 h (Test 1), 2 d (Test 2), and 6 d (Test 3) after training. On Test 1 the rats were either removed from the shock compartment immediately after entry or retained in the shock context for 200 sec, and intrahippocampal infusions of the protein synthesis inhibitor anisomycin (75 μg/side) were administered immediately after the test. Anisomycin infusions administered after Test 1 impaired IA performance on Test 2 in animals given the brief re-exposure, but impaired extinction in animals exposed to the context for 200 sec. Rats with anisomycin-induced retention impairment on Test 2 demonstrated spontaneous recovery of retention performance on Test 3, whereas rats showing extinction on Test 2 showed further extinction on Test 3. The findings indicate that post-retrieval administration of anisomycin impairs subsequent retention performance only in the absence of extinction and that this impairment is temporary.
机译:最近的研究报告了新的证据,该假设与以下假设一致:通过重新暴露于训练环境来重新激活记忆会破坏记忆的稳定性并引发“重新整合”。在本实验中,训练后6小时(测试1),2天(测试2)和6天(测试3)测试了大鼠的抑制回避(IA)训练记忆力。在试验1中,大鼠在进入后立即从休克隔室中取出,或在休克背景下停留200秒钟,并在试验后立即给予海马内蛋白质合成抑制剂茴香霉素(75μg/侧)输注。在进行短暂的再次暴露后,在测试1之后施用的茴香霉素输注会削弱动物在测试2上的IA性能,但会在暴露于环境200秒的动物体内造成灭绝的损害。在试验2中具有茴香霉素诱导的保留障碍的大鼠表现出在试验3中自发恢复了保留性能,而在试验2中显示灭绝的大鼠在试验3中显示了进一步消失。研究结果表明,取回后使用茴香霉素会损害随后的保留性能。没有灭绝,并且这种损害是暂时的。

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