Reconsolidation of a morphine place preference: Impact of the strength and age of memory on disruption by propranolol and midazolam

Robinson, Michael J.; Franklin, Keith B.J.

doi:10.1016/j.bbr.2010.04.056

Cited by 87 publications

(94 citation statements)

References 46 publications

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“…First, the protein synthesis reconsolidation-dependence is no longer necessary in the hippocampal CA3 area when memories are strong (asymptotic level of knowledge), suggesting that the strength of the memory is the key parameter for the need of the reconsolidation process. This result may explain some discrepancies described in previous studies about the age of the memory trace (Nader et al 2000;Milekic and Alberini 2002;Eisenberg and Dudai 2004;Suzuki et al 2004;Robinson and Franklin 2010) and this led us to draw a putative general model in which the strength of the memory could explain our results (Fig. 6A).…”

Section: Resultssupporting

confidence: 65%

“…First, memory age seems to be important and, over time, the memory trace seems to be less susceptible to disruption following its reactivation. This temporal gradient has been reported in very aversive associative tasks, such as passive avoidance and fear conditioning tasks (Milekic and Alberini 2002;Eisenberg and Dudai 2004;Suzuki et al 2004), but also in other behavioral tasks, such as the conditioned place preference task (Robinson and Franklin 2010) and drug-associated operant conditioning (Lee et al 2005). In these studies, the memory trace can be disrupted only a few days after its acquisition.…”

mentioning

confidence: 68%

“…For example, in the conditioned place preference task, amnestic treatments disrupted reconsolidation for weak memories (four pairings), but had little effect on stronger memories (eight pairings) reactivated 1 d after training (Robinson and Franklin 2010). In the fear conditioning task, an increase of training strength by increasing the number of CS -US associations makes the reactivated memory trace less susceptible to interference (Suzuki et al 2004;Lehmann and McNamara 2011).…”

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confidence: 99%

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Characterization of spatial memory reconsolidation

Jaeger¹,

Courtey²,

Brus³

et al. 2014

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Reconsolidation is necessary for the restabilization of reactivated memory traces. However, experimental parameters have been suggested as boundary conditions for this process. Here we investigated the role of a spatial memory trace's age, strength, and update on the reconsolidation process in mice. We first found that protein synthesis is necessary for reconsolidation to occur in the hippocampal CA3 region after reactivation of partially acquired and old memories but not for strongly acquired and recent memories. We also demonstrated that the update of a previously stable memory required, again, a memory reconsolidation in the hippocampal CA3. Finally, we found that the reactivation of a strongly acquired memory requires an activation of the anterior cingulate cortex as soon as 24 h after acquisition. This study demonstrates the importance of the knowledge of the task on the dynamic nature of memory reconsolidation processing.

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Section: Resultssupporting

confidence: 65%

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confidence: 68%

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confidence: 99%

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Characterization of spatial memory reconsolidation

Jaeger¹,

Courtey²,

Brus³

et al. 2014

Learn. Mem.

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“…Immediately after reactivation, half of the rats in each condition were administered Midazolam (MDZ, 3 mg/kg, i.p. ), a fast-acting positive modulator of the GABA-A receptor, known to disrupt memory reconsolidation of aversive and appetitive memories (Bustos et al 2006;Robinson and Franklin 2010;Stern et al 2012;De Oliveira Alvares et al 2013;Piñeyro et al 2014), while the other half received an equivalent amount of saline (SAL). To control for any unspecific effect of MDZ, a third condition was included in the experimental design.…”

Section: Methodsmentioning

confidence: 99%

An appetitive experience after fear memory destabilization attenuates fear retention: involvement GluN2B-NMDA receptors in the Basolateral Amygdala Complex

et al. 2016

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It is known that a consolidated memory can return to a labile state and become transiently malleable following reactivation. This instability is followed by a restabilization phase termed reconsolidation. In this work, we explored whether an unrelated appetitive experience (voluntary consumption of diluted sucrose) can affect a contextual fear memory in rats during the reactivation-induced destabilization phase. Our findings show that exposure to an appetitive experience following reactivation can diminish fear retention. This effect persisted after 1 wk. Importantly, it was achieved only under conditions that induced fear memory destabilization. This result could not be explained as a potentiated extinction, because sucrose was unable to promote extinction. Since GluN2B-containing NMDA receptors in the basolateral amygdala complex (BLA) have been implicated in triggering fear memory destabilization, we decided to block pharmacologically these receptors to explore the neurobiological bases of the observed effect. Intra-BLA infusion with ifenprodil, a GluN2B-NMDA antagonist, prevented the fear reduction caused by the appetitive experience. In sum, these results suggest that the expression of a fear memory can be dampened by an unrelated appetitive experience, as long as memory destabilization is achieved during reactivation. Possible mechanisms behind this effect and its clinical implications are discussed.

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“…For instance, extensive evidence suggests that pharmacological manipulations, such as giving protein synthesis inhibitors and adrenergic antagonists, can cause amnesia when given soon after a reactivation (Przybyslawski et al 1999;Nader et al 2000;Debiec et al 2002;Duvarci et al 2008;Milton et al 2008;Robinson and Franklin 2010). Likewise, memory can be pharmacologically enhanced immediately following a reactivation (Tronson et al 2006).…”

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confidence: 99%

Repeatedly reactivated memories become more resistant to hippocampal damage

Lehmann¹,

McNamara²

2011

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We examined whether repeated reactivations of a context memory would prevent the typical amnesic effects of post-training damage to the hippocampus (HPC). Rats were given a single contextual fear-conditioning session followed by 10 reactivations, involving a brief return to the conditioning context (no shock). Subsequently, the rats received sham or complete lesions of the HPC. When tested for retention, the HPC rats that experienced the reactivations froze significantly more than nonreactivation HPC rats and did not significantly differ from their respective control group. These findings suggest that memory reactivations contribute to long-term memories becoming independent of the HPC.

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Reconsolidation of a morphine place preference: Impact of the strength and age of memory on disruption by propranolol and midazolam

Cited by 87 publications

References 46 publications

Characterization of spatial memory reconsolidation

Characterization of spatial memory reconsolidation

An appetitive experience after fear memory destabilization attenuates fear retention: involvement GluN2B-NMDA receptors in the Basolateral Amygdala Complex

Repeatedly reactivated memories become more resistant to hippocampal damage

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