Enhancement of fear memory by retrieval through reconsolidation

Fukushima, Hotaka; Zhang, Yue; Archbold, Georgia; Ishikawa, Rie; Nader, Karim; Kida, Satoshi

doi:10.7554/elife.02736

Cited by 84 publications

(96 citation statements)

References 43 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…However, another study (Coccoz et al, 2011) using a similar stressor found that this stressor, when applied after memory reactivation, strengthened the memory. Similar findings have been obtained in a number of other studies (Fukushima et al, 2014).…”

Section: Discussionsupporting

confidence: 92%

Sequential exposure to a combination of stressors blocks memory reconsolidation in Lymnaea

Dodd

Lukowiak

2015

Journal of Experimental Biology

View full text Add to dashboard Cite

Stress alters the formation of long-term memory (LTM) in Lymnaea. When snails are exposed to more than one stressor, however, how the memory is altered becomes complicated. Here, we investigated how multiple stressors applied in a specific pattern affect an aspect of memory not often studied in regards to stress -reconsolidation. We hypothesized that the application of a sequence of stressors would block the reconsolidation process. Reconsolidation occurs following activation of a previously formed memory. Sequential crowding and handling were used as the stressors to block reconsolidation. When the two stressors were sequentially presented immediately following memory activation, reconsolidation was blocked. However, if the sequential presentation of the stressors was delayed for 1 h after memory activation, reconsolidation was not blocked. That is, LTM was observed. Finally, presentation of either stressor alone did not block reconsolidation. Thus, stressors can block reconsolidation, which may be preferable to pharmacological manipulations.

show abstract

Section: Discussionsupporting

confidence: 92%

Sequential exposure to a combination of stressors blocks memory reconsolidation in Lymnaea

Dodd

Lukowiak

2015

Journal of Experimental Biology

View full text Add to dashboard Cite

show abstract

“…Interestingly, all three of these molecules seem to be specifically involved in extinction, but not in the initial acquisition of fear conditioning (Cain et al 2002;Marsicano et al 2002;Baumgärtel et al 2008;Havekes et al 2008). The three of them have also been reported to be required for memory destabilization during reconsolidation (Suzuki et al 2008;Kim et al 2011;De Oliveira Alvares et al 2013;Fukushima et al 2014), along with other mechanisms such as AMPA receptor endocytosis (Hong et al 2013) and protein degradation through the ubiquitin-proteasome system (Lee 2008;Lee et al 2008;Sol Fustiñana et al 2014). This is in line with the view that these molecular components could be part of a system involved in the labilization of synaptic plasticity established by consolidation of the original memory trace (Almeida-Corrêa and Amaral 2014).…”

Section: Discussionmentioning

confidence: 99%

“…Interestingly, all three mechanisms seem to interact in endocannabinoid-mediated LTD in the hippocampus, with calcineurin apparently integrating the postsynaptic activation signal provided by LVGCCs and the presynaptic signal mediated by CB1 receptors (Heifets et al 2008). Calcineurin has also been shown to activate downstream targets that can mediate synaptic depression phenomena, such as AMPA receptor endocytosis (Beattie et al 2000;Kim et al 2007) and protein degradation through the ubiquitin-proteasome system (Fukushima et al 2014). Notably, both of these …”

Section: Discussionmentioning

confidence: 99%

“…Moreover, CaN activity in the amygdala seems to be unaltered (Lin et al 2003a) or repressed during initial learning (Baumgärtel et al 2008), but both its activity (Lin et al 2003a) and protein content (Merlo et al 2014) in the amygdala and its nuclear content in the hippocampus (de la Fuente et al 2011) are increased after extinction. Finally, blockade of calcineurin activity in the hippocampus (de la Fuente et al 2011) or of its expression in the amygdala (Merlo et al 2014) can disrupt extinction of fear conditioning, and its inhibition in the amygdala interferes with memory destabilization during reconsolidation of an inhibitory avoidance memory (Fukushima et al 2014). Taken together, these results suggest that CaN seems to be more involved in labilization of an existing memory trace than in formation of a fear memory.…”

mentioning

confidence: 89%

See 1 more Smart Citation

Calcineurin inhibition blocks within-, but not between-session fear extinction in mice

et al. 2015

View full text Add to dashboard Cite

Memory extinction involves the formation of a new associative memory that inhibits a previously conditioned association. Nonetheless, it could also depend on weakening of the original memory trace if extinction is assumed to have multiple components. The phosphatase calcineurin (CaN) has been described as being involved in extinction but not in the initial consolidation of fear learning. With this in mind, we set to study whether CaN could have different roles in distinct components of extinction. Systemic treatment with the CaN inhibitors cyclosporin A (CsA) or FK-506, as well as i.c.v. administration of CsA, blocked within-session, but not between-session extinction or initial learning of contextual fear conditioning. Similar effects were found in multiple-session extinction of contextual fear conditioning and in auditory fear conditioning, indicating that CaN is involved in different types of short-term extinction. Meanwhile, inhibition of protein synthesis by cycloheximide (CHX) treatment did not affect within-session extinction, but disrupted fear acquisition and slightly impaired between-session extinction. Our results point to a dissociation of within-and between-session extinction of fear conditioning, with the former being more dependent on CaN activity and the latter on protein synthesis. Moreover, the modulation of within-session extinction did not affect between-session extinction, suggesting that these components are at least partially independent.

show abstract

“…Previous work from our laboratory has demonstrated that IA memory can undergo reconsolidation dependent on mTOR activity in the hippocampus and amygdala after retrieval (Jobim et al 2012). Reconsolidation might serve to maintain (Jobim et al 2012) or strengthen (Fukushima et al 2014;Pedroso et al 2013) IA memory.…”

Section: Discussionmentioning

confidence: 88%

TrkB blockade in the hippocampus after training or retrieval impairs memory: protection from consolidation impairment by histone deacetylase inhibition

et al. 2015

View full text Add to dashboard Cite

Relatively little is known about the requirement of signaling initiated by brain-derived neurotrophic factor (BDNF) and its receptor, tropomyosin receptor kinase B (TrkB), in the early phases of memory consolidation, as well as about its possible functional interactions with epigenetic mechanisms. Here we show that blocking TrkB in the dorsal hippocampus after learning or retrieval impairs retention of memory for inhibitory avoidance (IA). More importantly, the impairing effect of TrkB antagonism on consolidation was completely prevented by the histone deacetylase (HDAC) inhibitor sodium butyrate (NaB). Male Wistar rats were given an intrahippocampal infusion of saline (SAL) or NaB before training, followed by an infusion of either vehicle (VEH) or the selective TrkB antagonist ANA-12 immediately after training. In a second experiment, the infusions were administered before and after retrieval. ANA-12 after either training or retrieval produced a significant impairment in a subsequent memory retention test. Pretraining administration of NaB prevented the effect of ANA-12, although NaB given before retrieval did not alter the impairment resulting from TrkB blockade. The results indicate that inhibition of BDNF/TrkB in the hippocampus can hinder consolidation and reconsolidation of IA memory. However, TrkB activity is not required for consolidation in the presence of NaB, suggesting that a dysfunction in BDNF/TrkB signaling can be fully compensated by HDAC inhibition to allow hippocampal memory formation.

show abstract

Enhancement of fear memory by retrieval through reconsolidation

Cited by 84 publications

References 43 publications

Sequential exposure to a combination of stressors blocks memory reconsolidation in Lymnaea

Sequential exposure to a combination of stressors blocks memory reconsolidation in Lymnaea

Calcineurin inhibition blocks within-, but not between-session fear extinction in mice

TrkB blockade in the hippocampus after training or retrieval impairs memory: protection from consolidation impairment by histone deacetylase inhibition

Contact Info

Product

Resources

About