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回忆后对海马体蛋白质合成的抑制会破坏痕迹条件反射中情景样记忆的表达。

Inhibition of hippocampal protein synthesis following recall disrupts expression of episodic-like memory in trace conditioning.

作者信息

Runyan Jason D, Dash Pramod K

机构信息

The Vivian L. Smith Center for Neurologic Research and Department of Neurobiology and Anatomy, University of Texas, Houston, Texas 77225, USA.

出版信息

Hippocampus. 2005;15(3):333-9. doi: 10.1002/hipo.20055.

Abstract

Transition of short-term to long-term memory is referred to as consolidation and the process is dependent on protein synthesis. Recently, several studies have shown that expression of consolidated memory for simple forms of learning tasks (e.g., delay conditioning, contextual fear, inhibitory avoidance) becomes vulnerable to disruption by inhibition of protein synthesis when administered shortly after recall. In the present study, we address whether recall-induced dependence on protein synthesis is a fundamental property that can be applied to a form of memory requiring attentional awareness or is specific to memories for simple forms of conditioning. Trace fear conditioning is a form of learning that requires an active memory trace to associate a conditioned stimulus (CS) with an unconditioned stimulus (US) separated by time. Our data demonstrate that whether a CS-alone recall trial in a novel context acts as an extinction or reactivation trial depends on the strength of the original memory. Inhibition of protein synthesis following the recall trial in animals receiving one trace conditioning training session (that gives rise to weak memory) resulted in enhanced CS-elicited freezing compared with vehicle control, as a result of impaired extinction memory, but had no effect on contextual memory. However, inhibition of hippocampal protein synthesis following the recall trial in animals receiving two trace conditioning training sessions (that gives rise to stronger memory) resulted in impaired retention of both trace CS-US associative and contextual memory despite that the context-US association was not directly reactivated. This provides evidence that, for a robust memory, the CS-alone recall trial results in the reactivation of an episodic-like memory, including trace CS- and contextual-memory, and that hippocampal information storage for the memory as a whole is returned to a labile state requiring de novo protein synthesis. This and other studies are consistent with the role of the hippocampus in coordinating episodic memory retrieval.

摘要

短期记忆向长期记忆的转变被称为巩固,这一过程依赖于蛋白质合成。最近,多项研究表明,对于简单形式的学习任务(如延迟条件反射、情境恐惧、抑制性回避),巩固记忆的表达在回忆后不久给予蛋白质合成抑制剂时,容易受到干扰。在本研究中,我们探讨回忆诱导的对蛋白质合成的依赖性是一种可应用于需要注意力意识的记忆形式的基本特性,还是特定于简单条件反射形式的记忆。痕迹恐惧条件反射是一种学习形式,需要一个活跃的记忆痕迹来将条件刺激(CS)与间隔一定时间的非条件刺激(US)联系起来。我们的数据表明,在新环境中单独进行的CS回忆试验是作为消退试验还是重新激活试验,取决于原始记忆的强度。在接受一次痕迹条件反射训练(产生较弱记忆)的动物中,回忆试验后抑制蛋白质合成,与给予载体对照相比,由于消退记忆受损,导致CS诱发的僵住增强,但对情境记忆没有影响。然而,在接受两次痕迹条件反射训练(产生较强记忆)的动物中,回忆试验后抑制海马体蛋白质合成,尽管情境-US关联未被直接重新激活,但导致痕迹CS-US联想记忆和情境记忆的保持均受损。这提供了证据,即对于稳固的记忆,单独的CS回忆试验会导致类似情节记忆的重新激活,包括痕迹CS记忆和情境记忆,并且整个记忆的海马体信息存储会恢复到需要重新进行蛋白质合成的不稳定状态。这项研究以及其他研究与海马体在协调情节记忆检索中的作用是一致的。

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