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给予蛋白合成抑制剂在提示之前会导致恢复由 NMDA 谷氨酸受体拮抗剂引起的记忆再巩固障碍导致的健忘症。

Protein synthesis inhibitor administration before a reminder caused recovery from amnesia induced by memory reconsolidation impairment with NMDA glutamate receptor antagonist.

机构信息

P.K. Anokhin Institute of Normal Physiology, 125315, Baltiyskaya Street, 8, Moscow, Russia.

出版信息

Brain Res Bull. 2021 Jun;171:44-55. doi: 10.1016/j.brainresbull.2021.03.008. Epub 2021 Mar 12.

Abstract

Memory recovery in amnestic animals is one of the most poorly studied processes. In this paper, we examine the role of protein synthesis and a reminder in the mechanisms of amnesia and memory recovery in grape snails trained to conditioned food aversion. Amnesia was induced by the impairment of memory reconsolidation using NMDA (N-methyl d-aspartate) glutamate receptor antagonists. In an early stage of amnesia (day 3), injections of protein synthesis inhibitors into animals combined with a reminder by a conditioned stimulus (CS) led to the recovery of aversive reactions to its presentation. Two types of changes in reactions to CS were revealed. In most animals, a persistent recovery of memory retrieval was found that lasted for at least 10 days. In other snails, aversive responses to CS persisted for 24 h. Isolated injections of inhibitors, injections of inhibitors and a reminder by the learning environment (without presenting a CS), usage of a differentiating stimulus instead of a CS, or inhibitor injections after the reminder did not affect the development of amnesia. The administration of protein synthesis inhibitors and a reminder in the late period after amnesia induction (10 days) did not affect its development or caused a short-term memory recovery. We suggest that amnesia is an active process that develops over time. The reminder induces the reactivation of the amnesia process dependent on protein synthesis, while the administration of protein synthesis inhibitors leads to the impairment of amnesia reactivation and recovery of the state formed before amnesia induction (i.e., recovery of conditioned food aversion memory).

摘要

记忆恢复在健忘动物中是研究最少的过程之一。在本文中,我们研究了蛋白质合成和提示在葡萄蜗牛条件性食物厌恶训练中遗忘和记忆恢复机制中的作用。通过使用 NMDA(N-甲基-D-天冬氨酸)谷氨酸受体拮抗剂损害记忆再巩固来诱导健忘。在健忘的早期(第 3 天),将蛋白质合成抑制剂注入动物体内并结合条件刺激(CS)的提示,导致对其呈现的厌恶反应恢复。揭示了对 CS 的反应的两种类型的变化。在大多数动物中,发现持久的记忆检索恢复持续至少 10 天。在其他蜗牛中,对 CS 的厌恶反应持续了 24 小时。单独注射抑制剂、抑制剂注射和学习环境的提示(不呈现 CS)、使用区分刺激而不是 CS、或在提示后进行抑制剂注射均不会影响健忘的发展。在健忘诱导后(10 天)的晚期给予蛋白质合成抑制剂和提示不会影响其发展或导致短期记忆恢复。我们认为健忘是一个随着时间的推移而发展的主动过程。提示诱导依赖于蛋白质合成的健忘过程的重新激活,而蛋白质合成抑制剂的给予导致健忘再激活的损伤和健忘诱导前形成的状态的恢复(即,条件性食物厌恶记忆的恢复)。

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