BDNF controls object recognition memory reconsolidation

Radiske, Andressa; Rossato, Janine I.; Gonzalez, María Carolina; Köhler, Cristiano A.; Bevilaqua, Lia R.; Cammarota, Martı́n

doi:10.1016/j.nlm.2017.02.018

Cited by 54 publications

(41 citation statements)

References 47 publications

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“…The expression levels of Bdnf and Zif268 in the mPFC and dorsal hippocampus were not affected by the retrieval of alcohol memories, contrary to the previous reports about the involvement of these genes in memory reconsolidation (Bozon et al, 2003;Lee et al, 2004;Tedesco et al, 2014;Radiske et al, 2015;Radiske et al, 2017). It is very likely that we did not observe this effect, because in our study the levels of the Bdnf and Zif268 mRNA were assessed 90 min after alcohol memory retrieval (since mice were also counterconditioned).…”

Section: Counterconditioning Manipulationcontrasting

confidence: 95%

“…Next, we assessed the mRNA expression of Zif268 and Bdnf, genes implicated in memory processing (Lee et al, 2004;Lee et al, 2005;Tedesco et al, 2014;Radiske et al, 2015;Radiske et al, 2017). We chose to focus on the mPFC and dorsal hippocampus, known to be involved in memory reconsolidation (Bozon et al, 2003;Lee et al, 2004;Tedesco et al, 2014;Radiske et al, 2015;Radiske et al, 2017), and in formation and expression of CPP or CPA (Zavala et al, 2003;Zhou and Zhu, 2006;Zarrindast et al, 2010;Chen et al, 2013;Otis et al, 2014;Slaker et al, 2015). Mice were trained in the alcohol-CPP procedure (Figure 2A; experimental design), and showed preference for the alcohol-paired compartment (Baseline test vs Place preference test 1 [t(22)=9.66, p<0.00001]).…”

Section: Bdnf Expression In the Mpfcmentioning

confidence: 99%

“…Specifically, we tested whether aversive counterconditioning of the alcohol-associated cues/context, conducted shortly after the retrieval of alcohol memories, can prevent reinstatement of alcohol-conditioned place preference (CPP) in mice, or renewal of alcohol seeking in an operant self-administration paradigm in rats. We also investigated the molecular correlates of the memory replacement mechanism, by assessing the expression of brain-derived-neurotrophic factor (Bdnf) and zinc-finger protein 268 (Zif268), genes previously implicated in memory processing (Lee et al, 2004;Lee et al, 2005;Tedesco et al, 2014;Radiske et al, 2015;Radiske et al, 2017), in the brain regions associated with memory reconsolidation.…”

Section: Introductionmentioning

confidence: 99%

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Disruption of relapse to alcohol seeking by aversive counterconditioning following memory retrieval

Goltseker

Handrus

Barak

2019

Preprint

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Relapse to alcohol abuse is often caused by exposure to potent alcohol-associated cues. Therefore, disruption of the cue-alcohol memory can prevent relapse. It is believed that memories destabilize and become prone for updating upon their reactivation through retrieval, and then re-stabilize within 6 h during a "reconsolidation" process. We recently showed that relapse to cocaine seeking could be prevented by counterconditioning the cocaine-cues with aversive outcomes following cocaine-memory retrieval, in a place conditioning paradigm. However, to better model addictionrelated behaviors, self-administration models are necessary. Here, we demonstrate that relapse to alcohol seeking can be prevented by aversive counterconditioning conducted during alcoholmemory reconsolidation, in conditioned place preference (CPP) and operant self-administration paradigms, in mice and rats, respectively. We found that the reinstatement of alcohol-CPP was abolished only when aversive counterconditioning with water-flooding was given shortly after alcohol-memory retrieval. Furthermore, rats trained to lever-press for alcohol showed decreased context-induced renewal of alcohol-seeking responding when the lever-pressing was counterconditioned with foot-shocks, shortly, but not 6 h, after memory retrieval. These results 0suggest that aversive counterconditioning can prevent relapse to alcohol seeking only when performed during alcohol-memory reconsolidation, presumably by updating, or replacing, the alcohol memory with aversive information. Also, we found that aversive counterconditioning preceded by alcohol-memory retrieval was characterized by upregulation of brain-derived neurotrophic factor (Bdnf) mRNA expression in the medial prefrontal cortex, suggesting that Bdnf plays a role in the memory updating process. Operant self-administration, Conditioned place preference, BDNFAlcohol place conditioning (days 2-9): Training started 24 h after the Baseline test with one session per day over 8 days, with the sliding door closed. On days 3, 5, 7, and 9, mice were administered with alcohol (1.8 g/kg; i.p.) and immediately confined to the paired compartment for 5 min. On the alternate days (days 2, 4, 6, and 8), mice were administered with saline and were confined to the unpaired compartment for the same duration as on the alcohol-conditioning day.Paired compartments were counterbalanced.Place preference test 1 (day 10): Place preference test was identical to the Baseline stage, and served to index alcohol-CPP (Cunningham et al., 2003). Preference was defined as an increase in the percent of time spent in the alcohol-paired compartment during the Place preference test 1 compared to the Baseline test. Mice that did not show CPP (minimum of 5% change) were excluded from the experiment (3 from Experiment 1; 4 from Experiment 2).Memory retrieval and aversive counterconditioning (days 11-14). Prior to this stage, mice were assigned to different experimental conditions, Retrieval and No Retrieval (matched for CPP scores and sex). Training began 2...

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Section: Counterconditioning Manipulationcontrasting

confidence: 95%

Section: Bdnf Expression In the Mpfcmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Disruption of relapse to alcohol seeking by aversive counterconditioning following memory retrieval

Goltseker

Handrus

Barak

2019

Preprint

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“…However, ORM reconsolidation only recruits this brain region when memory RA occurs concomitantly with novelty detection (Rossato et al, 2007;Winters et al, 2011). When induced by presentation of a novel object, reconsolidation mediates integration of new information into the reactivated ORM trace and is controlled by BDNF (Radiske et al, 2017b) and accompanied by a brief early post-RA depotentiation period followed by a late stage of synaptic efficacy enhancement (Clarke et al, 2010). Because PKM controls the facilitatory effect of BDNF on hippocampal LTP (Mei et al, 2011) and both PKM and BDNF regulate AMPAR surface expression during synaptic potentiation (Caldeira et al, 2007;Yao et al, 2008;Jourdi and Kabbaj, 2013), which seems necessary for reconsolidation (Rao-Ruiz et al, 2011;Bhattacharya et al, 2017), we hypothesized that PKM modulates ORM reconsolidation by mediating the interplay between BDNF and AMPAR recycling, so its inhibition after retrieval in the presence of a novel object impairs ORM reconsolidation and causes amnesia by deleting the reactivated recognition memory trace.…”

Section: Introductionmentioning

confidence: 99%

PKMζ Inhibition Disrupts Reconsolidation and Erases Object Recognition Memory

et al. 2019

Self Cite

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Object recognition memory (ORM) confers the ability to discriminate the familiarity of previously encountered items. Reconsolidation is the process by which reactivated memories become labile and susceptible to modifications. The hippocampus is specifically engaged in reconsolidation to integrate new information into the original ORM through a mechanism involving activation of brain-derived neurotrophic factor (BDNF) signaling and induction of LTP. It is known that BDNF can control LTP maintenance through protein kinase M (PKM), an atypical protein kinase C isoform that is thought to sustain memory storage by modulating glutamatergic neurotransmission. However, the potential involvement of PKM in ORM reconsolidation has never been studied. Using a novel ORM task combined with pharmacological, biochemical, and electrophysiological tools, we found that hippocampal PKM is essential to update ORM through reconsolidation, but not to maintain the inactive recognition memory trace stored over time, in adult male Wistar rats. Our results also indicate that hippocampal PKM acts downstream of BDNF and controls AMPAR synaptic insertion to elicit reconsolidation and suggest that blocking PKM activity during this process deletes active ORM.

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“…This is the first instance of experimental evidence showing that felbamate has promoting effects on the BDNF system. It is known that BDNF has a lot of physiological effects in the brain, playing critical roles in learning and memory, hippocampal neurogenesis, neuronal survival, and many others [44][45][46][47][48]. BDNF is implicated in the pathophysiology of many neurological disorders in addition to depression, such as Alzheimer's disease and Parkinson's disease [48][49][50][51][52].…”

Section: Discussionmentioning

confidence: 99%

Felbamate produces antidepressant‐like actions in the chronic unpredictable mild stress and chronic social defeat stress models of depression

Wang

Chen

et al. 2019

Fundamemntal Clinical Pharma

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Felbamate is an anticonvulsant used in the treatment of epilepsy. In this study, we investigated the antidepressant‐like actions of felbamate in mice. The effects of felbamate were first assessed using the forced swimming test (FST) and tail suspension test (TST), and then investigated in the chronic unpredictable mild stress (CUMS) and chronic social defeat stress (CSDS) models of depression. The changes in the hippocampal brain‐derived neurotrophic factor (BDNF) signaling cascade after chronic stress and felbamate treatment were also examined. It was found that felbamate exhibited antidepressant‐like activities in the FST and TST without affecting the locomotor activity of mice. Felbamate was also effective in both the CUMS and CSDS models of depression. Moreover, felbamate administration fully restored the decreased hippocampal BDNF signaling pathway in both the CUMS‐stressed and CSDS‐stressed mice. Collectively, felbamate has antidepressant‐like actions in mice involving the hippocampal BDNF system.

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BDNF controls object recognition memory reconsolidation

Cited by 54 publications

References 47 publications

Disruption of relapse to alcohol seeking by aversive counterconditioning following memory retrieval

Disruption of relapse to alcohol seeking by aversive counterconditioning following memory retrieval

PKMζ Inhibition Disrupts Reconsolidation and Erases Object Recognition Memory

Felbamate produces antidepressant‐like actions in the chronic unpredictable mild stress and chronic social defeat stress models of depression

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