Ethanol Enhances Reactivated Fear Memories

Nomura, Hiroshi; Matsuki, Norio

doi:10.1038/npp.2008.13

Cited by 37 publications

(29 citation statements)

References 44 publications

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“…In various training paradigms, strychnine, glucose, amphetamine or ethanol injections, when administered just after reactivation, have been shown to increase retention performance 24 or 48 h later. (Gordon and Spear 1973b;Rodriguez et al 1999;Blaiss and Janak 2006;Nomura and Matsuki 2008). Similar results have been obtained with more specific treatments, such as activating protein kinase A within the amygdala (Tronson et al 2006) or NMDA receptors (Lee et al 2006).…”

Section: Reactivation Allows the Facilitation Of Well-consolidated Mesupporting

confidence: 72%

Memory reactivation effects independent of reconsolidation

Gisquet-Verrier¹,

Riccio²

2012

Learn. Mem.

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Memory reactivation is an important process resulting from reexposure to salient training-related information whereby a memory is brought from an inactive to an active state. Reactivation is the first stage of memory retrieval but can result from the exposure to salient cues without any behavioral output. Such cue-induced reactivation, although frequently used by neuroscientists to study reconsolidation, has seldom been considered as a process in its own right and studied as such. This review presents arguments indicating that memory reactivation has two main consequences: (1) to enhance the accessibility of the target memory and (2) to make the memory malleable. Accordingly, reactivation creates a transient state during which the content of the memory is easily accessible and can be modified and/or updated. As both of these aspects can be observed shortly after memory reactivation, this review emphasizes that reconsolidation is not necessarily required for these processes and calls attention to reactivation as a factor in the dynamics of the memory.Memory retrieval is a complex (multistage) process through which previously acquired information can be used, leading to a behavioral output. Memory reactivation is the first component of retrieval corresponding to the process through which a memory is triggered from a latent state to a state in which it can be retrieved. Reactivation is generated by cues that are either external or self-generated and occurs in two general conditions. First, reactivation is required for retrieval and for every operation that enlarges or modifies previous knowledge. This includes retraining, when coherent supplementary information is provided, extinction when the previously learned response is no longer reinforced, and more generally, all rule-shiftings, i.e., when the contingency governing the response is changed. As a result, reactivation is largely embedded with retrieval and this probably explains why these two terms are often used interchangeably in the literature.

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Section: Reactivation Allows the Facilitation Of Well-consolidated Mesupporting

confidence: 72%

Memory reactivation effects independent of reconsolidation

Gisquet-Verrier¹,

Riccio²

2012

Learn. Mem.

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“…Taking into account the absence of an emotive charge in our paradigm and the doses selected, we wondered if this type of modulation during re-stabilization would induce a memory enhancement, as has been shown in other reports (Nomura and Matsuki, 2008).…”

Section: Introductionmentioning

confidence: 91%

“…Additionally, in this case, the effect of the drug did not differ between high-and low-anxiety rats. Interestingly, based on the well-known pharmacological actions of ethanol as a positive modulator of GABA A receptors (Lister, 1987;Weiss and Porrino, 2002), a recent study showed that ethanol, administered after the reactivation of a contextual fear memory, enhanced the performance of treated animals at testing (Nomura and Matsuki, 2008). Moreover, this effect appeared to be mediated by the GABAergic system because the administration of picrotoxin, a GABA A receptor antagonist, inhibited the memory enhancement produced by ethanol.…”

Section: Introductionmentioning

confidence: 96%

Enhancing a declarative memory in humans: The effect of clonazepam on reconsolidation

et al. 2013

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“…The memory retrieval and testing sessions consisted of exposing the mice to the condi-1 tioning chamber for 5 min in the absence of a footshock. All sessions were performed between 8 a.m. and 11 a.m., and each session was video-recorded for automatic scoring of freezing, according to a previously described method (Nomura and Matsuki 2008). Fear memory was assessed and expressed as the percentage of time the animal remained frozen-a commonly used parameter for measuring conditioned fear in mice.…”

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confidence: 99%

Post-retrieval late process contributes to persistence of reactivated fear memory

et al. 2013

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Several studies have demonstrated the mechanisms involved in memory persistence after learning. However, little is known about memory persistence after retrieval. In this study, a protein synthesis inhibitor, anisomycin, was infused into the basolateral amygdala of mice 9.5 h after retrieval of contextual conditioned fear. Anisomycin attenuated fear memory after 7 d, but not after 2 d. In contrast, infusion of anisomycin 5-or 24-h post-retrieval was ineffective. These findings indicate that anisomycin attenuates the persistence of reactivated fear memory in a time-dependent manner. We propose that late protein synthesis is required for memory persistence after retrieval.The process of memory formation is accompanied by protein synthesis, and various studies have demonstrated that the formation of long-term fear memory is disrupted by inhibiting protein synthesis around the time of learning or shortly afterward (Rosenblum et al. 1993;Bourtchouladze et al. 1998;McGaugh 2000;Johansen et al. 2011). During memory consolidation, protein synthesis is required to transform newly learned information, acquired during the acquisition phase, into stable modifications.While the molecular mechanisms involved in the acquisition and consolidation phases have been extensively studied, little is known about memory persistence. Recent studies have shown that late protein synthesis after learning is required for memory persistence (Bekinschtein et al. 2007;Rossato et al. 2009), suggesting that consolidation-like events take place again. This was highlighted in one study by Bekinschtein et al. (2007), whereby infusion of the protein synthesis inhibitor anisomycin into the dorsal hippocampus 12 h after learning disrupted memory persistence, but not memory formation.Several studies have shown that when a stabilized memory is retrieved, it can become labile again, and its maintenance requires additional protein synthesis (Nader et al. 2000;Debiec et al. 2002;Parsons et al. 2006a;Cai et al. 2012). Thus, this process is referred to as reconsolidation. Previous findings suggest that the reconsolidation phase involves many of the same core molecular features as the consolidation phase, including transcription factors (Kida et al. 2002), and de novo mRNA and protein synthesis (Nader et al. 2000;Debiec et al. 2002;Da Silva et al. 2008;Duvarci et al. 2008). However, no studies have explicated how memory persists after retrieval. It remains unclear whether persistence of retrieved memory requires a late protein synthesis-dependent phase as the persistence of original memory does. We aimed to clarify this in the present study.To this end, we used contextual fear conditioning, employing footshock as our aversive stimulus. Our study focused on the basolateral amygdala (BLA), an area of the brain critical for the formation and maintenance of memory associated with fear (Phillips and LeDoux 1992; LeDoux 2000; Gale et al. 2004;Rudy et al. 2004;Poulos et al. 2009;Nomura et al. 2012). It has been shown that protein synthesis in the amygdala is necessa...

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Ethanol Enhances Reactivated Fear Memories

Cited by 37 publications

References 44 publications

Memory reactivation effects independent of reconsolidation

Memory reactivation effects independent of reconsolidation

Enhancing a declarative memory in humans: The effect of clonazepam on reconsolidation

Post-retrieval late process contributes to persistence of reactivated fear memory

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