Memory reconsolidation and amnesia induction: Separate processes dependent on specific protein and RNA synthesis.

IF 1.6 4区 医学 Q3 BEHAVIORAL SCIENCES
Vladimir P Nikitin, Svetlana V Solntseva, Pavel V Nikitin
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引用次数: 0

Abstract

The reconsolidation hypothesis posits that memory retrieval initiates a phase of memory destabilization, followed by restabilization through protein synthesis-dependent processes. The disruption of reconsolidation by amnestic agents can lead to memory loss. Yet, this hypothesis leaves unanswered questions regarding the mechanisms driving amnesia induction and reversal of molecular and structural changes underlying memory retention. Our previous work proposed that amnesia induction is an active process reliant on both translation and transcription. To test this hypothesis, we explored the role of N-methyl-D-aspartate (NMDA) glutamate receptors, as well as protein and RNA synthesis in amnesia induction mechanisms in grape snails trained with conditional food aversion, during the initial hours following memory reconsolidation disruption. Our results reveal that protein synthesis inhibitor administration before the conditioned reminder stimulus caused amnesia 3 hr after the reminder, whereas NMDA glutamate receptor antagonists resulted in amnesia less than 20 min following the first conditioned reminder stimulus. Concurrent administration of an NMDA receptor antagonist and a protein synthesis inhibitor before the reminder resulted in a rapid (less than 20 min) and complete prevention of amnesia, underscoring the pivotal role of protein synthesis in NMDA-dependent amnesia induction. Conversely, RNA synthesis inhibitors did not affect memory reconsolidation but inhibited amnesia triggered by an NMDA receptor antagonist. Moreover, our study demonstrates a significant difference in the dependency of memory reconsolidation and amnesia induction "time windows" on protein synthesis. These findings lend support to our hypothesis that memory reconsolidation and amnesia represent distinct processes, each characterized by unique developmental dynamics and molecular underpinnings. (PsycInfo Database Record (c) 2024 APA, all rights reserved).

记忆再巩固和失忆诱导:依赖于特定蛋白质和 RNA 合成的独立过程
重新巩固假说认为,记忆检索会启动一个记忆不稳定阶段,然后通过依赖蛋白质合成的过程重新稳定记忆。失忆剂对再巩固过程的破坏会导致记忆丧失。然而,这一假说对失忆诱导和逆转记忆保持的分子和结构变化的驱动机制留下了悬而未决的问题。我们之前的研究提出,失忆诱导是一个依赖于翻译和转录的活跃过程。为了验证这一假设,我们探索了 N-甲基-D-天冬氨酸(NMDA)谷氨酸受体以及蛋白质和 RNA 合成在记忆再巩固中断后最初几小时内对葡萄蜗牛进行条件性食物厌恶训练的失忆诱导机制中的作用。我们的研究结果表明,在条件性提醒刺激之前服用蛋白质合成抑制剂会导致提醒后 3 小时的失忆,而 NMDA 谷氨酸受体拮抗剂会导致第一次条件性提醒刺激后不到 20 分钟的失忆。在催眠之前同时服用 NMDA 受体拮抗剂和蛋白质合成抑制剂可迅速(不到 20 分钟)完全防止失忆,这强调了蛋白质合成在 NMDA 依赖性失忆诱导中的关键作用。相反,RNA合成抑制剂不影响记忆的再巩固,但抑制了NMDA受体拮抗剂引发的失忆。此外,我们的研究表明,记忆再巩固和失忆诱导 "时间窗 "对蛋白质合成的依赖性存在显著差异。这些发现支持了我们的假设,即记忆再巩固和失忆代表了不同的过程,各自具有独特的发育动态和分子基础。(PsycInfo Database Record (c) 2024 APA, 版权所有)。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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来源期刊
Behavioral neuroscience
Behavioral neuroscience 医学-行为科学
CiteScore
3.40
自引率
0.00%
发文量
51
审稿时长
6-12 weeks
期刊介绍: Behavioral Neuroscience publishes original research articles as well as reviews in the broad field of the neural bases of behavior.
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