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Ivan Izquierdo - One of the best experts on this subject based on the ideXlab platform.
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Molecular Mechanisms in Hippocampus Involved on Object Recognition Memory Consolidation and Reconsolidation.
Neuroscience, 2020Co-Authors: Cristiane Regina Guerino Furini, Jociane De Carvalho Myskiw, Eduarda Godfried Nachtigall, Jonny Anderson Kielbovicz Behling, Eduardo Silva De Assis Brasil, Bruna Freitas Saenger, Rodrigo F. Narvaes, Ivan IzquierdoAbstract:Abstract Acquired information is stabilized into long-term Memory through a process known as consolidation. Though, after consolidation, when stored information is retrieved they can be again susceptible, allowing modification, updating and strengthening and to be re-stabilized they need a new process referred to as Memory reconsolidation. However, the molecular mechanisms of Recognition Memory consolidation and reconsolidation are not fully understood. Also, considering that the study of the link between synaptic proteins is key to understanding of Memory processes, we investigated, in male Wistar rats, molecular mechanisms in the hippocampus involved on Object Recognition Memory (ORM) consolidation and reconsolidation. We verified that the blockade of AMPA receptors (AMPAr) and L-VDCCs calcium channels impaired ORM consolidation and reconsolidation when administered into CA1 immediately after sample phase or reactivation phase and that these impairments were blocked by the administration of AMPAr agonist and of neurotrophin BDNF. Also, the blockade of CaMKII impaired ORM consolidation when administered 3 h after sample phase but had no effect on ORM reconsolidation and its effect was blocked by the administration of BDNF, but not of AMPAr agonist. So, this study provides new evidence of the molecular mechanisms involved on the consolidation and reconsolidation of ORM, demonstrating that AMPAr and L-VDCCs are necessary for the consolidation and reconsolidation of ORM while CaMKII is necessary only for the consolidation and also that there is a link between BDNF and AMPAr, L-VDCCs and CaMKII as well as a link between AMPAr and L-VDCCs on ORM consolidation and reconsolidation.
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The relationship between protein synthesis and protein degradation in Object Recognition Memory
2016Co-Authors: Cristiane Regina Guerino Furini, Jociane De Carvalho Myskiw, Bianca E. Schmidt, Carolina G. Zinn, Patricia B. Peixoto, Luiza Doro Pereira, Ivan IzquierdoAbstract:For decades there has been a consensus that de novo protein synthesis is necessary for long-term Memory. A second round of protein synthesis has been described for both extinction and reconsolidation. Recently, it was demonstrated that consolidation and reconsolidation depend not only on protein synthesis but also on protein degradation by the ubiquitin-proteasome system (UPS). However, the involvement of UPS on consolidation and reconsolidation of Object Recognition Memory (OR) remains unclear.
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The relationship between protein synthesis and protein degradation in Object Recognition Memory
Behavioural brain research, 2015Co-Authors: Cristiane Regina Guerino Furini, Jociane De Carvalho Myskiw, Bianca E. Schmidt, Carolina G. Zinn, Patricia B. Peixoto, Luiza Doro Pereira, Ivan IzquierdoAbstract:For decades there has been a consensus that de novo protein synthesis is necessary for long-term Memory. A second round of protein synthesis has been described for both extinction and reconsolidation following an unreinforced test session. Recently, it was shown that consolidation and reconsolidation depend not only on protein synthesis but also on protein degradation by the ubiquitin-proteasome system (UPS), a major mechanism responsible for protein turnover. However, the involvement of UPS on consolidation and reconsolidation of Object Recognition Memory remains unknown. Here we investigate in the CA1 region of the dorsal hippocampus the involvement of UPS-mediated protein degradation in consolidation and reconsolidation of Object Recognition Memory. Animals with infusion cannulae stereotaxically implanted in the CA1 region of the dorsal hippocampus, were exposed to an Object Recognition task. The UPS inhibitor β-Lactacystin did not affect the consolidation and the reconsolidation of Object Recognition Memory at doses known to affect other forms of Memory (inhibitory avoidance, spatial learning in a water maze) while the protein synthesis inhibitor anisomycin impaired the consolidation and the reconsolidation of the Object Recognition Memory. However, β-Lactacystin was able to reverse the impairment caused by anisomycin on the reconsolidation process in the CA1 region of the hippocampus. Therefore, it is possible to postulate a direct link between protein degradation and protein synthesis during the reconsolidation of the Object Recognition Memory.
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The role of histamine receptors in the consolidation of Object Recognition Memory.
Neurobiology of learning and memory, 2013Co-Authors: Clarice Kras Borges Da Silveira, Cristiane Regina Guerino Furini, Fernando Benetti, Siomara Monteiro, Ivan IzquierdoAbstract:Findings have shown that histamine receptors in the hippocampus modulate the acquisition and extinction of fear motivated learning. In order to determine the role of hippocampal histaminergic receptors on Recognition Memory, adult male Wistar rats with indwelling infusion cannulae stereotaxically placed in the CA1 region of dorsal hippocampus were trained in an Object Recognition learning task involving exposure to two different stimulus Objects in an enclosed environment. In the test session, one of the Objects presented during training was replaced by a novel one. Recognition Memory retention was assessed 24 h after training by comparing the time spent in exploration (sniffing and touching) of the known Object with that of the novel one. When infused in the CA1 region immediately, 30, 120 or 360 min posttraining, the H1-receptor antagonist, pyrilamine, the H2-receptor antagonist, ranitidine, and the H3-receptor agonist, imetit, blocked long-term Memory retention in a time dependent manner (30–120 min) without affecting general exploratory behavior, anxiety state or hippocampal function. Our data indicate that histaminergic system modulates consolidation of Object Recognition Memory through H1, H2 and H3 receptors.
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Decreased acetylcholine release delays the consolidation of Object Recognition Memory.
Behavioural brain research, 2012Co-Authors: Xavier De Jaeger, Ivan Izquierdo, Martin Cammarota, Marco A. M. Prado, Vania F. Prado, Grace S. PereiraAbstract:Acetylcholine (ACh) is important for different cognitive functions such as learning, Memory and attention. The release of ACh depends on its vesicular loading by the vesicular acetylcholine transporter (VAChT). It has been demonstrated that VAChT expression can modulate Object Recognition Memory. However, the role of VAChT expression on Object Recognition Memory persistence still remains to be understood. To address this question we used distinct mouse lines with reduced expression of VAChT, as well as pharmacological manipulations of the cholinergic system. We showed that reduction of cholinergic tone impairs Object Recognition Memory measured at 24h. Surprisingly, Object Recognition Memory, measured at 4 days after training, was impaired by substantial, but not moderate, reduction in VAChT expression. Our results suggest that levels of acetylcholine release strongly modulate Object Recognition Memory consolidation and appear to be of particular importance for Memory persistence 4 days after training.
Cristiane Regina Guerino Furini - One of the best experts on this subject based on the ideXlab platform.
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Molecular Mechanisms in Hippocampus Involved on Object Recognition Memory Consolidation and Reconsolidation.
Neuroscience, 2020Co-Authors: Cristiane Regina Guerino Furini, Jociane De Carvalho Myskiw, Eduarda Godfried Nachtigall, Jonny Anderson Kielbovicz Behling, Eduardo Silva De Assis Brasil, Bruna Freitas Saenger, Rodrigo F. Narvaes, Ivan IzquierdoAbstract:Abstract Acquired information is stabilized into long-term Memory through a process known as consolidation. Though, after consolidation, when stored information is retrieved they can be again susceptible, allowing modification, updating and strengthening and to be re-stabilized they need a new process referred to as Memory reconsolidation. However, the molecular mechanisms of Recognition Memory consolidation and reconsolidation are not fully understood. Also, considering that the study of the link between synaptic proteins is key to understanding of Memory processes, we investigated, in male Wistar rats, molecular mechanisms in the hippocampus involved on Object Recognition Memory (ORM) consolidation and reconsolidation. We verified that the blockade of AMPA receptors (AMPAr) and L-VDCCs calcium channels impaired ORM consolidation and reconsolidation when administered into CA1 immediately after sample phase or reactivation phase and that these impairments were blocked by the administration of AMPAr agonist and of neurotrophin BDNF. Also, the blockade of CaMKII impaired ORM consolidation when administered 3 h after sample phase but had no effect on ORM reconsolidation and its effect was blocked by the administration of BDNF, but not of AMPAr agonist. So, this study provides new evidence of the molecular mechanisms involved on the consolidation and reconsolidation of ORM, demonstrating that AMPAr and L-VDCCs are necessary for the consolidation and reconsolidation of ORM while CaMKII is necessary only for the consolidation and also that there is a link between BDNF and AMPAr, L-VDCCs and CaMKII as well as a link between AMPAr and L-VDCCs on ORM consolidation and reconsolidation.
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The relationship between protein synthesis and protein degradation in Object Recognition Memory
2016Co-Authors: Cristiane Regina Guerino Furini, Jociane De Carvalho Myskiw, Bianca E. Schmidt, Carolina G. Zinn, Patricia B. Peixoto, Luiza Doro Pereira, Ivan IzquierdoAbstract:For decades there has been a consensus that de novo protein synthesis is necessary for long-term Memory. A second round of protein synthesis has been described for both extinction and reconsolidation. Recently, it was demonstrated that consolidation and reconsolidation depend not only on protein synthesis but also on protein degradation by the ubiquitin-proteasome system (UPS). However, the involvement of UPS on consolidation and reconsolidation of Object Recognition Memory (OR) remains unclear.
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The relationship between protein synthesis and protein degradation in Object Recognition Memory
Behavioural brain research, 2015Co-Authors: Cristiane Regina Guerino Furini, Jociane De Carvalho Myskiw, Bianca E. Schmidt, Carolina G. Zinn, Patricia B. Peixoto, Luiza Doro Pereira, Ivan IzquierdoAbstract:For decades there has been a consensus that de novo protein synthesis is necessary for long-term Memory. A second round of protein synthesis has been described for both extinction and reconsolidation following an unreinforced test session. Recently, it was shown that consolidation and reconsolidation depend not only on protein synthesis but also on protein degradation by the ubiquitin-proteasome system (UPS), a major mechanism responsible for protein turnover. However, the involvement of UPS on consolidation and reconsolidation of Object Recognition Memory remains unknown. Here we investigate in the CA1 region of the dorsal hippocampus the involvement of UPS-mediated protein degradation in consolidation and reconsolidation of Object Recognition Memory. Animals with infusion cannulae stereotaxically implanted in the CA1 region of the dorsal hippocampus, were exposed to an Object Recognition task. The UPS inhibitor β-Lactacystin did not affect the consolidation and the reconsolidation of Object Recognition Memory at doses known to affect other forms of Memory (inhibitory avoidance, spatial learning in a water maze) while the protein synthesis inhibitor anisomycin impaired the consolidation and the reconsolidation of the Object Recognition Memory. However, β-Lactacystin was able to reverse the impairment caused by anisomycin on the reconsolidation process in the CA1 region of the hippocampus. Therefore, it is possible to postulate a direct link between protein degradation and protein synthesis during the reconsolidation of the Object Recognition Memory.
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The role of histamine receptors in the consolidation of Object Recognition Memory.
Neurobiology of learning and memory, 2013Co-Authors: Clarice Kras Borges Da Silveira, Cristiane Regina Guerino Furini, Fernando Benetti, Siomara Monteiro, Ivan IzquierdoAbstract:Findings have shown that histamine receptors in the hippocampus modulate the acquisition and extinction of fear motivated learning. In order to determine the role of hippocampal histaminergic receptors on Recognition Memory, adult male Wistar rats with indwelling infusion cannulae stereotaxically placed in the CA1 region of dorsal hippocampus were trained in an Object Recognition learning task involving exposure to two different stimulus Objects in an enclosed environment. In the test session, one of the Objects presented during training was replaced by a novel one. Recognition Memory retention was assessed 24 h after training by comparing the time spent in exploration (sniffing and touching) of the known Object with that of the novel one. When infused in the CA1 region immediately, 30, 120 or 360 min posttraining, the H1-receptor antagonist, pyrilamine, the H2-receptor antagonist, ranitidine, and the H3-receptor agonist, imetit, blocked long-term Memory retention in a time dependent manner (30–120 min) without affecting general exploratory behavior, anxiety state or hippocampal function. Our data indicate that histaminergic system modulates consolidation of Object Recognition Memory through H1, H2 and H3 receptors.
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Infusion of protein synthesis inhibitors in the entorhinal cortex blocks consolidation but not reconsolidation of Object Recognition Memory.
Neurobiology of learning and memory, 2009Co-Authors: Ramón H. Lima, Janine I Rossato, Lia R M Bevilaqua, Ivan Izquierdo, Cristiane Regina Guerino Furini, Martin CammarotaAbstract:Memory consolidation and reconsolidation require the induction of protein synthesis in some areas of the brain. Here, we show that infusion of the protein synthesis inhibitors anisomycin, emetine and cycloheximide in the entorhinal cortex immediately but not 180 min or 360 min after training in an Object Recognition learning task hinders long-term Memory retention without affecting short-term Memory or behavioral performance. Inhibition of protein synthesis in the entorhinal cortex after Memory reactivation involving either a combination of familiar and novel Objects or two familiar Objects does not affect retention. Our data suggest that protein synthesis in the entorhinal cortex is necessary early after training for consolidation of Object Recognition Memory. However, inhibition of protein synthesis in this cortical region after Memory retrieval does not seem to affect the stability of the Recognition trace.
Timothy J. Bussey - One of the best experts on this subject based on the ideXlab platform.
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Object Recognition Memory neurobiological mechanisms of encoding consolidation and retrieval
Neuroscience & Biobehavioral Reviews, 2008Co-Authors: Boyer D. Winters, Lisa M. Saksida, Timothy J. BusseyAbstract:Abstract Tests of Object Recognition Memory, or the judgment of the prior occurrence of an Object, have made substantial contributions to our understanding of the nature and neurobiological underpinnings of mammalian Memory. Only in recent years, however, have researchers begun to elucidate the specific brain areas and neural processes involved in Object Recognition Memory. The present review considers some of this recent research, with an emphasis on studies addressing the neural bases of perirhinal cortex-dependent Object Recognition Memory processes. We first briefly discuss operational definitions of Object Recognition and the common behavioural tests used to measure it in non-human primates and rodents. We then consider research from the non-human primate and rat literature examining the anatomical basis of Object Recognition Memory in the delayed nonmatching-to-sample (DNMS) and spontaneous Object Recognition (SOR) tasks, respectively. The results of these studies overwhelmingly favor the view that perirhinal cortex (PRh) is a critical region for Object Recognition Memory. We then discuss the involvement of PRh in the different stages – encoding, consolidation, and retrieval – of Object Recognition Memory. Specifically, recent work in rats has indicated that neural activity in PRh contributes to Object Memory encoding, consolidation, and retrieval processes. Finally, we consider the pharmacological, cellular, and molecular factors that might play a part in PRh-mediated Object Recognition Memory. Recent studies in rodents have begun to indicate the remarkable complexity of the neural substrates underlying this seemingly simple aspect of declarative Memory.
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Scopolamine infused into perirhinal cortex improves Object Recognition Memory by blocking the acquisition of interfering Object information.
Learning & memory (Cold Spring Harbor N.Y.), 2007Co-Authors: Boyer D. Winters, Lisa M. Saksida, Susan J. Bartko, Timothy J. BusseyAbstract:In a previous study, we reported apparently paradoxical facilitation of Object Recognition Memory following infusions of the cholinergic muscarinic receptor antagonist scopolamine into the perirhinal cortex (PRh) of rats. We attributed these effects to the blockade by scopolamine of the acquisition of interfering information. The present study tested this possibility directly by modifying the spontaneous Object Recognition Memory task to allow the presentation of a potentially interfering Object either before the sample phase or in the retention delay between the sample and choice phases. Presentation of an Object between the sample and choice phases disrupted subsequent Recognition of the sample Object (retroactive interference), and intra-PRh infusions of scopolamine prior to the presentation of the irrelevant Object prevented this retroactive interference effect. Moreover, presentation of an irrelevant Object prior to the sample phase interfered proactively with sample Object Recognition, and intra-PRh infusions of scopolamine prior to the presentation of the pre-sample Object prevented this proactive interference effect. These results suggest that blocking muscarinic cholinergic receptors in PRh can disrupt the acquisition of potentially interfering Object information, thereby facilitating Object Recognition Memory. This finding provides further, strong evidence that acetylcholine is important for the acquisition of Object information in PRh.
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why does brain damage impair Memory a connectionist model of Object Recognition Memory in perirhinal cortex
The Journal of Neuroscience, 2006Co-Authors: Rosemary A Cowell, Timothy J. Bussey, Lisa M. SaksidaAbstract:Object Recognition is the canonical test of declarative Memory, the type of Memory putatively impaired after damage to the temporal lobes. Studies of Object Recognition Memory have helped elucidate the anatomical structures involved in declarative Memory, indicating a critical role for perirhinal cortex. We offer a mechanistic account of the effects of perirhinal cortex damage on Object Recognition Memory, based on the assumption that perirhinal cortex stores representations of the conjunctions of visual features possessed by complex Objects. Such representations are proposed to play an important role in Memory when it is difficult to solve a task using representations of only individual visual features of stimuli, thought to be stored in regions of the ventral visual stream caudal to perirhinal cortex. The account is instantiated in a connectionist model, in which development of Object representations with visual experience provides a mechanism for judgment of previous occurrence. We present simulations addressing the following empirical findings: (1) that impairments after damage to perirhinal cortex (modeled by removing the “perirhinal cortex” layer of the network) are exacerbated by lengthening the delay between presentation of to-be-remembered items and test, (2) that such impairments are also exacerbated by lengthening the list of to-be-remembered items, and (3) that impairments are revealed only when stimuli are trial unique rather than repeatedly presented. This study shows that it may be possible to account for Object Recognition impairments after damage to perirhinal cortex within a hierarchical, representational framework, in which complex conjunctive representations in perirhinal cortex play a critical role.
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glutamate receptors in perirhinal cortex mediate encoding retrieval and consolidation of Object Recognition Memory
The Journal of Neuroscience, 2005Co-Authors: Boyer D. Winters, Timothy J. BusseyAbstract:Object Recognition is consistently impaired in human amnesia and animal models thereof. Results from subjects with permanent brain damage have revealed the importance of the perirhinal cortex to Object Recognition Memory. Here, we report evidence from rats for interdependent but distinct stages in Object Recognition Memory (encoding, retrieval, and consolidation), which require glutamate receptor activity within perirhinal cortex. Transient blockade of AMPA receptor-mediated synaptic transmission within perirhinal cortex disrupted encoding for short- and long-term Memory as well as retrieval and consolidation. In contrast, transient NMDA receptor blockade during encoding affected only long-term Object Recognition Memory; NMDA receptor activity was also necessary for consolidation but not retrieval. These results further demonstrate the importance of perirhinal cortex for Object Recognition Memory and suggest that, as in the hippocampus, AMPA and NMDA receptors mediate synaptic transmission and activity-dependent synaptic plasticity, respectively, in several stages of Memory processing.
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transient inactivation of perirhinal cortex disrupts encoding retrieval and consolidation of Object Recognition Memory
The Journal of Neuroscience, 2005Co-Authors: Boyer D. Winters, Timothy J. BusseyAbstract:Damage to perirhinal cortex (PRh) impairs Object Recognition Memory in humans, monkeys, and rats when tested in tasks such as delayed nonmatching to sample, visual paired comparison, and its rodent analog, the spontaneous Object Recognition task. In the present study, we have capitalized on the discrete one-trial nature of the spontaneous Object Recognition task to investigate the role of PRh in several distinct stages of Object Recognition Memory. In a series of experiments, transient inactivation of PRh was accomplished with bilateral infusions of lidocaine directly into PRh immediately before the sample phase (encoding), immediately before the choice phase (retrieval), or within the retention delay after the sample phase (storage-consolidation). Compared with performance on trials in which they received saline infusions, rats were significantly impaired when lidocaine was infused before the sample phase, regardless of the length of the retention delay. Similarly, delay-independent deficits were observed after immediate pre-choice infusions of lidocaine. Finally, PRh inactivation immediately and 20 min after the sample phase, but not 40, 60, or 80 min after, also disrupted subsequent Object Recognition when the retention delay was sufficiently long to ensure the dissipation of the actions of lidocaine during the choice phase. The effects of pre-sample and pre-choice inactivation indicate involvement of PRh in encoding and retrieval stages of Object Recognition, and the time course of post-sample inactivation effects suggests a role for PRh in the maintenance of the Object trace during Memory consolidation.
Martin Cammarota - One of the best experts on this subject based on the ideXlab platform.
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PKMζ Inhibition Disrupts Reconsolidation and Erases Object Recognition Memory.
The Journal of neuroscience : the official journal of the Society for Neuroscience, 2019Co-Authors: Janine I Rossato, Lia R M Bevilaqua, Andressa Radiske, Maria Carolina Gonzalez, Gênedy K.s. Apolinário, Sergio A. Conde-ocazionez, Martin CammarotaAbstract: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 Mζ (PKMζ), an atypical protein kinase C isoform that is thought to sustain Memory storage by modulating glutamatergic neurotransmission. However, the potential involvement of PKMζ in ORM reconsolidation has never been studied. Using a novel ORM task combined with pharmacological, biochemical, and electrophysiological tools, we found that hippocampal PKMζ 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 PKMζ acts downstream of BDNF and controls AMPAR synaptic insertion to elicit reconsolidation and suggest that blocking PKMζ activity during this process deletes active ORM.SIGNIFICANCE STATEMENT Object Recognition Memory (ORM) is essential to remember facts and events. Reconsolidation integrates new information into ORM through changes in hippocampal plasticity and brain-derived neurotrophic factor (BDNF) signaling. In turn, BDNF enhances synaptic efficacy through protein kinase Mζ (PKMζ), which might preserve Memory. Here, we present evidence that hippocampal PKMζ acts downstream of BDNF to regulate AMPAR recycling during ORM reconsolidation and show that this kinase is essential to update the reactivated Recognition Memory trace, but not to consolidate or maintain an inactive ORM. We also demonstrate that the amnesia provoked by disrupting ORM reconsolidation through PKMζ inhibition is due to Memory erasure and not to retrieval failure.
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BDNF controls Object Recognition Memory reconsolidation.
Neurobiology of learning and memory, 2017Co-Authors: Andressa Radiske, Janine I Rossato, Lia R M Bevilaqua, Maria Carolina Gonzalez, Cristiano A. Köhler, Martin CammarotaAbstract:Reconsolidation restabilizes Memory after reactivation. Previously, we reported that the hippocampus is engaged in Object Recognition Memory reconsolidation to allow incorporation of new information into the original engram. Here we show that BDNF is sufficient for this process, and that blockade of BDNF function in dorsal CA1 impairs updating of the reactivated Recognition Memory trace.
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Decreased acetylcholine release delays the consolidation of Object Recognition Memory.
Behavioural brain research, 2012Co-Authors: Xavier De Jaeger, Ivan Izquierdo, Martin Cammarota, Marco A. M. Prado, Vania F. Prado, Grace S. PereiraAbstract:Acetylcholine (ACh) is important for different cognitive functions such as learning, Memory and attention. The release of ACh depends on its vesicular loading by the vesicular acetylcholine transporter (VAChT). It has been demonstrated that VAChT expression can modulate Object Recognition Memory. However, the role of VAChT expression on Object Recognition Memory persistence still remains to be understood. To address this question we used distinct mouse lines with reduced expression of VAChT, as well as pharmacological manipulations of the cholinergic system. We showed that reduction of cholinergic tone impairs Object Recognition Memory measured at 24h. Surprisingly, Object Recognition Memory, measured at 4 days after training, was impaired by substantial, but not moderate, reduction in VAChT expression. Our results suggest that levels of acetylcholine release strongly modulate Object Recognition Memory consolidation and appear to be of particular importance for Memory persistence 4 days after training.
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Infusion of protein synthesis inhibitors in the entorhinal cortex blocks consolidation but not reconsolidation of Object Recognition Memory.
Neurobiology of learning and memory, 2009Co-Authors: Ramón H. Lima, Janine I Rossato, Lia R M Bevilaqua, Ivan Izquierdo, Cristiane Regina Guerino Furini, Martin CammarotaAbstract:Memory consolidation and reconsolidation require the induction of protein synthesis in some areas of the brain. Here, we show that infusion of the protein synthesis inhibitors anisomycin, emetine and cycloheximide in the entorhinal cortex immediately but not 180 min or 360 min after training in an Object Recognition learning task hinders long-term Memory retention without affecting short-term Memory or behavioral performance. Inhibition of protein synthesis in the entorhinal cortex after Memory reactivation involving either a combination of familiar and novel Objects or two familiar Objects does not affect retention. Our data suggest that protein synthesis in the entorhinal cortex is necessary early after training for consolidation of Object Recognition Memory. However, inhibition of protein synthesis in this cortical region after Memory retrieval does not seem to affect the stability of the Recognition trace.
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on the role of hippocampal protein synthesis in the consolidation and reconsolidation of Object Recognition Memory
Learning & Memory, 2007Co-Authors: Janine I Rossato, Lia R M Bevilaqua, Jociane De Carvalho Myskiw, Jorge H Medina, Ivan Izquierdo, Martin CammarotaAbstract:Upon retrieval, consolidated memories are again rendered vulnerable to the action of metabolic blockers, notably protein synthesis inhibitors. This has led to the hypothesis that memories are reconsolidated at the time of retrieval, and that this depends on protein synthesis. Ample evidence indicates that the hippocampus plays a key role both in the consolidation and reconsolidation of different memories. Despite this fact, at present there are no studies about the consequences of hippocampal protein synthesis inhibition in the storage and post-retrieval persistence of Object Recognition Memory. Here we report that infusion of the protein synthesis inhibitor anisomycin in the dorsal CA1 region immediately or 180 min but not 360 min after training impairs consolidation of long-term Object Recognition Memory without affecting short-term Memory, exploratory behavior, anxiety state, or hippocampal functionality. When given into CA1 after Memory reactivation in the presence of familiar Objects, ANI did not affect further retention. However, when administered into CA1 immediately after exposing animals to a novel and a familiar Object, ANI impaired Memory of both of them. The amnesic effect of ANI was long-lasting, did not happen after exposure to two novel Objects, following exploration of the context alone, or in the absence of specific stimuli, suggesting that it was not reversible but was contingent on the reactivation of the consolidated trace in the presence of a salient, behaviorally relevant novel cue. Our results indicate that hippocampal protein synthesis is required during a limited post-training time window for consolidation of Object Recognition Memory and show that the hippocampus is engaged during reconsolidation of this type of Memory, maybe accruing new information into the original trace.
Jociane De Carvalho Myskiw - One of the best experts on this subject based on the ideXlab platform.
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Molecular Mechanisms in Hippocampus Involved on Object Recognition Memory Consolidation and Reconsolidation.
Neuroscience, 2020Co-Authors: Cristiane Regina Guerino Furini, Jociane De Carvalho Myskiw, Eduarda Godfried Nachtigall, Jonny Anderson Kielbovicz Behling, Eduardo Silva De Assis Brasil, Bruna Freitas Saenger, Rodrigo F. Narvaes, Ivan IzquierdoAbstract:Abstract Acquired information is stabilized into long-term Memory through a process known as consolidation. Though, after consolidation, when stored information is retrieved they can be again susceptible, allowing modification, updating and strengthening and to be re-stabilized they need a new process referred to as Memory reconsolidation. However, the molecular mechanisms of Recognition Memory consolidation and reconsolidation are not fully understood. Also, considering that the study of the link between synaptic proteins is key to understanding of Memory processes, we investigated, in male Wistar rats, molecular mechanisms in the hippocampus involved on Object Recognition Memory (ORM) consolidation and reconsolidation. We verified that the blockade of AMPA receptors (AMPAr) and L-VDCCs calcium channels impaired ORM consolidation and reconsolidation when administered into CA1 immediately after sample phase or reactivation phase and that these impairments were blocked by the administration of AMPAr agonist and of neurotrophin BDNF. Also, the blockade of CaMKII impaired ORM consolidation when administered 3 h after sample phase but had no effect on ORM reconsolidation and its effect was blocked by the administration of BDNF, but not of AMPAr agonist. So, this study provides new evidence of the molecular mechanisms involved on the consolidation and reconsolidation of ORM, demonstrating that AMPAr and L-VDCCs are necessary for the consolidation and reconsolidation of ORM while CaMKII is necessary only for the consolidation and also that there is a link between BDNF and AMPAr, L-VDCCs and CaMKII as well as a link between AMPAr and L-VDCCs on ORM consolidation and reconsolidation.
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The relationship between protein synthesis and protein degradation in Object Recognition Memory
2016Co-Authors: Cristiane Regina Guerino Furini, Jociane De Carvalho Myskiw, Bianca E. Schmidt, Carolina G. Zinn, Patricia B. Peixoto, Luiza Doro Pereira, Ivan IzquierdoAbstract:For decades there has been a consensus that de novo protein synthesis is necessary for long-term Memory. A second round of protein synthesis has been described for both extinction and reconsolidation. Recently, it was demonstrated that consolidation and reconsolidation depend not only on protein synthesis but also on protein degradation by the ubiquitin-proteasome system (UPS). However, the involvement of UPS on consolidation and reconsolidation of Object Recognition Memory (OR) remains unclear.
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The relationship between protein synthesis and protein degradation in Object Recognition Memory
Behavioural brain research, 2015Co-Authors: Cristiane Regina Guerino Furini, Jociane De Carvalho Myskiw, Bianca E. Schmidt, Carolina G. Zinn, Patricia B. Peixoto, Luiza Doro Pereira, Ivan IzquierdoAbstract:For decades there has been a consensus that de novo protein synthesis is necessary for long-term Memory. A second round of protein synthesis has been described for both extinction and reconsolidation following an unreinforced test session. Recently, it was shown that consolidation and reconsolidation depend not only on protein synthesis but also on protein degradation by the ubiquitin-proteasome system (UPS), a major mechanism responsible for protein turnover. However, the involvement of UPS on consolidation and reconsolidation of Object Recognition Memory remains unknown. Here we investigate in the CA1 region of the dorsal hippocampus the involvement of UPS-mediated protein degradation in consolidation and reconsolidation of Object Recognition Memory. Animals with infusion cannulae stereotaxically implanted in the CA1 region of the dorsal hippocampus, were exposed to an Object Recognition task. The UPS inhibitor β-Lactacystin did not affect the consolidation and the reconsolidation of Object Recognition Memory at doses known to affect other forms of Memory (inhibitory avoidance, spatial learning in a water maze) while the protein synthesis inhibitor anisomycin impaired the consolidation and the reconsolidation of the Object Recognition Memory. However, β-Lactacystin was able to reverse the impairment caused by anisomycin on the reconsolidation process in the CA1 region of the hippocampus. Therefore, it is possible to postulate a direct link between protein degradation and protein synthesis during the reconsolidation of the Object Recognition Memory.
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on the role of hippocampal protein synthesis in the consolidation and reconsolidation of Object Recognition Memory
Learning & Memory, 2007Co-Authors: Janine I Rossato, Lia R M Bevilaqua, Jociane De Carvalho Myskiw, Jorge H Medina, Ivan Izquierdo, Martin CammarotaAbstract:Upon retrieval, consolidated memories are again rendered vulnerable to the action of metabolic blockers, notably protein synthesis inhibitors. This has led to the hypothesis that memories are reconsolidated at the time of retrieval, and that this depends on protein synthesis. Ample evidence indicates that the hippocampus plays a key role both in the consolidation and reconsolidation of different memories. Despite this fact, at present there are no studies about the consequences of hippocampal protein synthesis inhibition in the storage and post-retrieval persistence of Object Recognition Memory. Here we report that infusion of the protein synthesis inhibitor anisomycin in the dorsal CA1 region immediately or 180 min but not 360 min after training impairs consolidation of long-term Object Recognition Memory without affecting short-term Memory, exploratory behavior, anxiety state, or hippocampal functionality. When given into CA1 after Memory reactivation in the presence of familiar Objects, ANI did not affect further retention. However, when administered into CA1 immediately after exposing animals to a novel and a familiar Object, ANI impaired Memory of both of them. The amnesic effect of ANI was long-lasting, did not happen after exposure to two novel Objects, following exploration of the context alone, or in the absence of specific stimuli, suggesting that it was not reversible but was contingent on the reactivation of the consolidated trace in the presence of a salient, behaviorally relevant novel cue. Our results indicate that hippocampal protein synthesis is required during a limited post-training time window for consolidation of Object Recognition Memory and show that the hippocampus is engaged during reconsolidation of this type of Memory, maybe accruing new information into the original trace.