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血管紧张素调节长臂虾的长期记忆表达,但不影响长期记忆储存。

Angiotensin modulates long-term memory expression but not long-term memory storage in the crab Chasmagnathus.

机构信息

Laboratorio de Neurobiología de la Memoria, Departamento de Fisiología y Biología Molecular, IFIByNE-CONICET, Pabellón II, FCEyN, Universidad de Buenos Aires, Ciudad Universitaria (C1428EHA), Argentina.

出版信息

Neurobiol Learn Mem. 2010 Nov;94(4):509-20. doi: 10.1016/j.nlm.2010.09.003. Epub 2010 Sep 7.

Abstract

Memory reconsolidation is a dynamic process in which a previously consolidated memory becomes labile following reactivation by a reminder. In a previous study in the crab Chasmagnathus memory model, we showed that a water-shortage episode, via angiotensin modulation during reconsolidation, could reveal a memory that otherwise remains unexpressed: weakly trained animals cannot reveal long-term memory (LTM) except when an episode of noticeable ethological meaning, water deprivation, is contingent upon reconsolidation. However, these results are at variance with two of our previous interpretations: weak training protocols do not build LTM and angiotensin II modulates the strength of the information storing process. A parsimonious hypothesis is that in Chasmagnathus angiotensins regulate LTM expression, but not LTM storage. Here, we tested three predictions of this hypothesis. First, the well-known retrograde amnesic effect of the angiotensin II antagonist saralasin is not due to interference on memory storage, but to modulation of memory expression. Second, the recovery of the LTM memory expression of the apparently amnesic retrograde effect produced by saralasin, through the water-shortage episode contingent upon reconsolidation, must be reconsolidation specific. Consequently, summation-like effects and retrieval deficits cannot explain these results because of the parametric conditions of reconsolidation. Third, weak training protocols build an unexpressed LTM that requires mRNA transcription and translation, a diagnostic characteristic of LTM. Results show that angiotensin modulates LTM expression but not LTM memory storage in the crab Chasmagnathus. The results lead us to suggest that, in Chasmagnathus, LTM expression - the process of gaining appreciable control over behavior of the reactivated trace in the retrieval session - may be considered a distinct attribute of its long-term storage. This strategy, a positive modulation during reconsolidation, is proposed to distinguish between memories that can be reactivated, labilized and are not expressed, and memories that are not stored long term, obliterated or altered in other retrieval mechanisms.

摘要

记忆再巩固是一个动态过程,其中先前巩固的记忆在被提醒重新激活后变得不稳定。在之前的螃蟹 Chasmagnathus 记忆模型的研究中,我们表明,通过再巩固期间的血管紧张素调节,缺水事件可以揭示否则未表达的记忆:弱训练动物不能揭示长期记忆 (LTM),除非在注意到的行为意义上的缺水事件与再巩固有关。然而,这些结果与我们之前的两个解释不一致:弱训练方案不会建立 LTM,血管紧张素 II 调节信息存储过程的强度。一个简洁的假设是,在 Chasmagnathus 中,血管紧张素调节 LTM 的表达,但不调节 LTM 的存储。在这里,我们测试了这个假设的三个预测。首先,血管紧张素 II 拮抗剂 saralasin 的众所周知的逆行性遗忘效应不是由于对记忆存储的干扰,而是由于对记忆表达的调节。其次,通过与再巩固有关的缺水事件,逆转效应产生的 LTM 记忆表达的恢复,必须是再巩固特异性的。因此,由于再巩固的参数条件,类似总和的效应和检索缺陷不能解释这些结果。第三,弱训练方案建立了一种未表达的 LTM,需要 mRNA 转录和翻译,这是 LTM 的一个诊断特征。结果表明,血管紧张素调节螃蟹 Chasmagnathus 的 LTM 表达,但不调节 LTM 记忆存储。这些结果使我们提出,在 Chasmagnathus 中,LTM 表达——即在检索过程中获得对被激活痕迹的显著控制的过程——可以被认为是其长期存储的一个独特属性。这种策略,即在再巩固期间进行积极的调节,旨在区分可以被重新激活、不稳定且未表达的记忆,以及不能长期存储、被抹去或在其他检索机制中改变的记忆。

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