Characterization of spatial memory reconsolidation

Jaeger, Xavier De; Courtey, Julie; Brus, Maïna; Artinian, Julien; Villain, Hélène; Bacquié, Elodie

doi:10.1101/lm.033415.113

Cited by 15 publications

(12 citation statements)

References 40 publications

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“…3). Accordingly, pharmacological, functional imaging, and lesioning studies indicate an important role for the dorsal hippocampus in the reconsolidation of contextual fear conditioning (Boccia et al 2010;Jobim et al 2012;Lee et al 2013;De Jaeger et al 2014). These findings may also be interpreted as additional evidence supporting a role for hippocampal NMDA receptors, particularly those containing the GluN2 subunit, in memory reconsolidation (Pedreira et al 2002;Lee et al 2006;Ribeiro et al 2013), as far as the agonist and the antagonist of the polyaminebinding site at the NMDAr improved and disrupted memory reconsolidation, respectively.…”

Section: Discussionmentioning

confidence: 80%

Spermidine-induced improvement of reconsolidation of memory involves calcium-dependent protein kinase in rats

et al. 2015

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In this study, we determined whether the calcium-dependent protein kinase (PKC) signaling pathway is involved in the improvement of fear memory reconsolidation induced by the intrahippocampal administration of spermidine in rats. Male Wistar rats were trained in a fear conditioning apparatus using a 0.4-mA footshock as an unconditioned stimulus. Twenty-four hours after training, animals were re-exposed to the apparatus in the absence of shock (reactivation session). Immediately after the reactivation session, spermidine (2 -200 pmol/site), the PKC inhibitor 3-[1-(dimethylaminopropyl)indol-3-yl]-4-(indol-3-yl) maleimide hydrochloride (GF 109203X, 0.3 -30 pg/site), the antagonist of the polyamine-binding site at the NMDA receptor, arcaine (0.2 -200 pmol/site), or the PKC activator phorbol 12-myristate 13-acetate (PMA, 0.02 -2 nmol/site) was injected. While the post-reactivation administration of spermidine (20 and 200 pmol/site) and PMA (2 nmol/site) improved memory reconsolidation, GF 109203X (1, 10, and 30 pg/site) and arcaine (200 pmol/site) impaired it. GF 109203X (0.3 pg/site) impaired memory reconsolidation in the presence of spermidine (200 pmol/site). PMA (0.2 nmol/site) prevented the arcaine (200 pmol/site)-induced impairment of memory reconsolidation. Anisomycin (2 mg/site) also impaired memory reconsolidation in the presence of spermidine (200 pmol/site). Drugs had no effect when they were administered in the absence of reactivation. These results suggest that the spermidine-induced enhancement of memory reconsolidation involves PKC activation.

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Section: Discussionmentioning

confidence: 80%

Spermidine-induced improvement of reconsolidation of memory involves calcium-dependent protein kinase in rats

et al. 2015

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“…For the reconsolidation procedure, 24 h after training, a reactivation trial (R) consisting in an additional learning trial, was performed (De Jaeger et al, 2014 ). The PT took place 24 h after reactivation.…”

Section: Methodsmentioning

confidence: 99%

Effects of Propranolol, a β-noradrenergic Antagonist, on Memory Consolidation and Reconsolidation in Mice

Villain

Benkahoul

Drougard

et al. 2016

Front. Behav. Neurosci.

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Memory reconsolidation impairment using the β-noradrenergic receptor blocker propranolol is a promising novel treatment avenue for patients suffering from pathogenic memories, such as post-traumatic stress disorder (PTSD). However, in order to better inform targeted treatment development, the effects of this compound on memory need to be better characterized via translational research. We examined the effects of systemic propranolol administration in mice undergoing a wide range of behavioral tests to determine more specifically which aspects of the memory consolidation and reconsolidation are impaired by propranolol. We found that propranolol (10 mg/kg) affected memory consolidation in non-aversive tasks (object recognition and object location) but not in moderately (Morris water maze (MWM) to highly (passive avoidance, conditioned taste aversion) aversive tasks. Further, propranolol impaired memory reconsolidation in the most and in the least aversive tasks, but not in the moderately aversive task, suggesting its amnesic effect was not related to task aversion. Moreover, in aquatic object recognition and location tasks in which animals were forced to behave (contrary to the classic versions of the tasks); propranolol did not impair memory reconsolidation. Taken together our results suggest that the memory impairment observed after propranolol administration may result from a modification of the emotional valence of the memory rather than a disruption of the contextual component of the memory trace. This is relevant to the use of propranolol to block memory reconsolidation in individuals with PTSD, as such a treatment would not erase the traumatic memory but only reduce the emotional valence associated with this event.

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“…The retrieval of a consolidated information may lead to a new labile phase making the reactivated memory malleable23. Through this mechanism, memories can be strengthened or updated, allowing new information to be integrated into the existing memory trace4.…”

mentioning

confidence: 99%

“…The processes of memory formation are dynamic and newly learned information stored in short term memory (STM) undergoes progressive changes and a stabilization process named as memory consolidation 1 . The retrieval of a consolidated information may lead to a new labile phase making the reactivated memory malleable 2 3 . Through this mechanism, memories can be strengthened or updated, allowing new information to be integrated into the existing memory trace 4 .…”

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confidence: 99%

HDAC inhibition promotes both initial consolidation and reconsolidation of spatial memory in mice

Villain

Florian

Roullet

2016

Sci Rep

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Accumulating evidence suggests a critical role for epigenetic regulations in long term memory (LTM) formation. Among them, post-translational modifications of proteins, as histone acetylation, are an important regulator of chromatin remodelling and gene transcription. While the implication of histone acetylation in memory consolidation is widely accepted, less is known about its role in memory reconsolidation i.e. during memory restabilization after its reactivation. In the present study, we investigated the role of histone acetylation during the initial consolidation and the reconsolidation of spatial memory, using a weak massed learning procedure in the Morris water maze paradigm in mice. Usually a weak learning is sufficient for short term memory (STM) formation, but insufficient to upgrade STM to LTM. We found that promoting histone acetylation through intra-hippocampal infusion of a class I selective histone deacetylase (HDAC) inhibitor immediately after a subthreshold spatial learning improved LTM but not STM retention. More importantly, inhibiting HDAC activity after the reactivation of a weak memory promoted specifically LTM reconsolidation without affecting post-reactivation STM. These findings argue in favour of an important role for histone acetylation in memory consolidation, and more particularly during the reconsolidation of spatial memory in mice.

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Characterization of spatial memory reconsolidation

Cited by 15 publications

References 40 publications

Spermidine-induced improvement of reconsolidation of memory involves calcium-dependent protein kinase in rats

Spermidine-induced improvement of reconsolidation of memory involves calcium-dependent protein kinase in rats

Effects of Propranolol, a β-noradrenergic Antagonist, on Memory Consolidation and Reconsolidation in Mice

HDAC inhibition promotes both initial consolidation and reconsolidation of spatial memory in mice

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