Reconsolidation of memory after its reactivation

Przybyslawski, J; Sara, Susan J.

doi:10.1016/s0166-4328(96)00153-2

Cited by 426 publications

(306 citation statements)

References 19 publications

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“…Thus, it has been demonstrated that Pavlovian associations require a protein synthesis-dependent "reconsolidation" (Nader et al, 2000). This reconsolidation may involve plasticity-related processes (Przybyslawski and Sara, 1997), and the selective changes in the regional expression of the plasticity-related gene ␥ PKC in those groups in which the light stimulus was associated with cocaine seen in the present study may form part of the molecular mechanism underlying the lasting storage of this Pavlovian association. Furthermore, the associative storage of input patterns to the NAcc may be mediated by the strengthening sets of prefrontal and amygdala inputs.…”

Section: Synthesissupporting

confidence: 53%

Limbic-Cortical-Ventral Striatal Activation during Retrieval of a Discrete Cocaine-Associated Stimulus: A Cellular Imaging Study with γ Protein Kinase C Expression

Thomas

Everitt

2001

J. Neurosci.

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We investigated the neuronal activation associated with reexposure to a discrete cocaine-associated stimulus using in situ hybridization to quantify the expression of the plasticityregulated gene, ␥ protein kinase C (␥ PKC), in the limbiccortical-ventral striatal system. Groups of rats were trained to self-administer cocaine paired with a light stimulus (Paired) or paired with an auditory stimulus but also receiving light presentations yoked to those in the Paired group (Unpaired). Additional groups received noncontingent cocaine-light pairings (Pavlovian) or saline-light pairings (Saline) that were yoked to the Paired group. After acquisition of self-administration by the Paired and Unpaired groups, all groups had a 3 d drug-and training-free period before being reexposed to noncontingent presentations of the light conditioning stimulus during a 5 min test session in the training context. There were four major patterns of results for regional ␥ PKC expression 2 hr later. (1) Changes occurred only in groups in which the light was predictive of cocaine. (2) Increases were seen in the amygdala, but decreases were seen in the medial prefrontal cortex. (3) No changes were seen in the hippocampus. (4) Although changes were observed in the basal and central nuclei of the amygdala and the prelimbic cortex in both the Paired and Pavlovian groups, additional changes were observed in the nucleus accumbens core, lateral amygdala, and anterior cingulate cortex in the Pavlovian group. These results suggest not only that regionally selective alterations in ␥ PKC expression are an index of the retrieval of Pavlovian associations formed between a drug and a discrete stimulus, but also that a distinct neural circuitry may underlie Pavlovian stimulus-reward associations in cocaine-experienced rats.

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Section: Synthesissupporting

confidence: 53%

Limbic-Cortical-Ventral Striatal Activation during Retrieval of a Discrete Cocaine-Associated Stimulus: A Cellular Imaging Study with γ Protein Kinase C Expression

Thomas

Everitt

2001

J. Neurosci.

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“…Since the reminder that induce reconsolidation is also a part of the cues presented during training, but the unconditioned stimulus (US) is not presented after the conditioned stimulus (CS), new information is available for being learned and other processes emerge as candidates for explaining any post-retrieval effect, like extinction (Myers and Davis, 2002). Standard controls determine that retention performance should not be affected if the treatment is administered in absence of memory reactivation or showing that the post-retrieval treatment needs to be given before the end of a temporal window to be effective (Alberini, 2011;Alberini, Milekic, & Tronel, 2006;Dudai, 2006;Misanin, Miller, & Lewis, 1968;Przybyslawski & Sara, 1997;Tronson & Taylor, 2007). However, none of these controls can completely discard that a new learning process is occurring, and that it is the actual responsible for performance in subsequent tests.…”

Section: Discussionmentioning

confidence: 99%

Choline reverses scopolamine-induced memory impairment by improving memory reconsolidation

Blake

Boccia

Krawczyk

et al. 2012

Neurobiology of Learning and Memory

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Please cite this article as: Blake, M.G., Boccia, M.M., Krawczyk, M.C., Delorenzi, A., Baratti, C.M., Choline reverses scopolamine-induced memory impairment by improving memory reconsolidation, Neurobiology of Learning and Memory (2012), doi: http://dx.doi. org/10.1016/j.nlm.2012.07.001 This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain. were not subjected to memory reactivation, suggesting that the performance effects are not due to non-specific effects of the drug. The effects of Ch also depended on the age of the reactivated memory. Altogether, our results suggest that Ch exerts its effects by modulating memory reconsolidation, and that the memory impairment induced by low doses of SCP is a memory expression failure and not a storage deficit. Therefore, reconsolidation, among other functions, might serve to change memory expression in later tests. Summarizing, our results open new avenues about the behavioral significance and the physiological functions of memory reconsolidation, providing new strategies for recovering memories from some types of amnesia. Research highlights-Pre-training administration of scopolamine leads to memory impairment.-Intra-hippocampal administration of choline modulates memory reconsolidation -Choline reverses scopolamine-induced amnesia by enhancing memory reconsolidation -Low doses of scopolamine cause memory expression deficit, but not storage impairment -Reconsolidation could modify the ability of a memory for being expressed later

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“…This result lends significant support to the current widely held view that reactivated old memories undergo a "reconsolidation" process to update the information. For the most part, the existence of reconsolidation processes have only been inferred from the fact that amnesia can be induced after reactivation of well established memories (Przybyslawski and Sara, 1997;Nader et al, 2000) (for review, see Sara, 2000;Nader, 2003;Dudai, 2006). If the learning-dependent increase in spindle density is, as it is purported to be, a physiological marker of off-line memory consolidation, then the increase seen after retrieval from remote memory may indeed indicate that a reconsolidation process is taking place.…”

Section: Discussionmentioning

confidence: 99%

Elevated Sleep Spindle Density after Learning or after Retrieval in Rats

Eschenko

Mölle²,

Born³

et al. 2006

J. Neurosci.

227

199

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Non-rapid eye movement sleep has been strongly implicated in consolidation of both declarative and procedural memory in humans. Elevated sleep-spindle density in slow-wave sleep after learning has been shown recently in humans. It has been proposed that sleep spindles, 12-15 Hz oscillations superimposed on slow waves (Ͻ1 Hz), in concert with high-frequency hippocampal sharp waves/ripples, promote neural plasticity underlying remote memory formation. The present study reports the first indication of learning-associated increase in spindle density in the rat, providing an animal model to study the role of brain oscillations in memory consolidation during sleep. An odor-reward association task, analogous in many respects to human paired-associate learning, is rapidly learned and leads to robust memory in rats. Rats learned the task over 10 massed trials within a single session, and EEG was monitored for 3 h after learning. Learning-induced increase in spindle density is reliably reproduced in rats in two different learning situations, differing primarily in the behavioral component of the task. This increase in spindle density is also present after reactivation of remote memory and in situations when memory update is required; it is not observed after noncontingent exposure to reward and training context. The latter results substantially extend findings in humans. The magnitude of increase (ϳ25%) and the time window of maximal effect (ϳ1 h after sleep onset) were remarkably similar to human data, making this a valid rodent model to study network interactions through the use of simultaneous unit recordings and local field potentials during postlearning sleep.

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Reconsolidation of memory after its reactivation

Cited by 426 publications

References 19 publications

Limbic-Cortical-Ventral Striatal Activation during Retrieval of a Discrete Cocaine-Associated Stimulus: A Cellular Imaging Study with γ Protein Kinase C Expression

Limbic-Cortical-Ventral Striatal Activation during Retrieval of a Discrete Cocaine-Associated Stimulus: A Cellular Imaging Study with γ Protein Kinase C Expression

Choline reverses scopolamine-induced memory impairment by improving memory reconsolidation

Elevated Sleep Spindle Density after Learning or after Retrieval in Rats

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