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Xing Liu - One of the best experts on this subject based on the ideXlab platform.
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β1-Adrenoceptor in the Central Amygdala Is Required for Unconditioned Stimulus-Induced Drug Memory Reconsolidation.
The international journal of neuropsychopharmacology, 2017Co-Authors: Huiwen Zhu, Yiming Zhou, Zhiyuan Liu, Xi Chen, Xing LiuAbstract:Background Drug memories become labile and reconsolidated after retrieval by presentation of environmental cues (conditioned stimulus) or drugs (unconditioned stimulus). Whether conditioned stimulus and unconditioned stimulus retrieval trigger different Memory Reconsolidation processes is not clear. Methods Protein synthesis inhibitor or β-adrenergic receptor (β-AR) antagonist was systemically administrated or intra-central amygdala infused immediately after cocaine reexposure in cocaine-conditioned place preference or self-administration mice models. β-ARs were selectively knocked out in the central amygdala to further confirm the role of β-adrenergic receptor in cocaine reexposure-induced Memory Reconsolidation of cocaine-conditioned place preference. Results Cocaine reexposure triggered de novo protein synthesis dependent Memory Reconsolidation of cocaine-conditioned place preference. Cocaine-priming-induced reinstatement was also impaired with post cocaine retrieval manipulation, in contrast to the relapse behavior with post context retrieval manipulation. Cocaine retrieval, but not context retrieval, induced central amygdala activation. Protein synthesis inhibitor or β1-adrenergic receptor antagonist infused in the central amygdala after cocaine retrieval, but not context retrieval, inhibited Memory Reconsolidation and reinstatement. β1-adrenergic receptor knockout in the central amygdala suppressed cocaine retrieval-triggered Memory Reconsolidation and reinstatement of cocaine conditioned place preference. β1-adrenergic receptor antagonism after cocaine retrieval also impaired Reconsolidation and reinstatement of cocaine self-administration. Conclusions Cocaine reward Memory triggered by unconditioned stimulus retrieval is distinct from conditioned stimulus retrieval. Unconditioned stimulus retrieval induced Reconsolidation of cocaine reward Memory depends on β1-adrenergic signaling in the central amygdala. Post unconditioned stimulus retrieval manipulation can prevent drug Memory Reconsolidation and relapse to cocaine, thus providing a potential strategy for the prevention of substance addiction. Significance statement It is well known that drug memories become labile and reconsolidated upon retrieval by the presentation of conditioned stimulus (CS) or unconditioned stimulus (US). Whether CS and US retrieval trigger different Memory Reconsolidation processes is unknown. In this study, we found that US retrieval, but not CS retrieval, triggered Memory Reconsolidation of cocaine-conditioned place preference dependent on β1-AR and de novo protein synthesis in the central amygdala. Furthermore, cocaine priming-induced reinstatement was impaired with post US retrieval manipulation in contrast to the relapse behavior with post CS retrieval manipulation. In cocaine self-administration, β1-AR antagonism after US retrieval also impaired Reconsolidation and reinstatement. Our study indicates that Reconsolidation of cocaine reward Memory triggered by US retrieval is distinct from CS retrieval. US retrieval induced Reconsolidation of cocaine reward Memory depends on β1-adrenergic signaling in the central amygdala.
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Unconditioned- and Conditioned- Stimuli Induce Differential Memory Reconsolidation and β-AR-Dependent CREB Activation.
Frontiers in neural circuits, 2017Co-Authors: Bing Huang, Huiwen Zhu, Yiming Zhou, Xing LiuAbstract:Consolidated long-term fear memories become labile and reconsolidated upon retrieval by the presentation of conditioned stimulus (CS) or unconditioned stimulus (US). Whether CS-retrieval or US-retrieval will trigger different Memory Reconsolidation processes is unknown. In this study, we introduced a sequential fear conditioning paradigm that Footshock was paired with two distinct Sounds. Propranolol, β-adrenergic receptor (β-AR) antagonist, treated after US-retrieval impaired freezing behavior evoked by CS-A and CS-B. Betaxolol, a selective β1-AR antagonist, showed the similar effects as propranolol. However, propranolol treatment after CS-retrieval only inhibited freezing behavior evoked by the same CS, i.e., CS-A (or CS-B), not the other CS. These data suggest that β-AR is critically involved in US-retrieval triggered Memory Reconsolidation of fear conditioning as CS-retrieval, and β-AR blockade after US-retrieval disrupts more CS-US associations than CS-retrieval does. Furthermore, US-retrieval induced significant CREB activation in almost the whole amygdala and hippocampus, but CS-retrieval only stimulated CREB activation in the lateral amygdala (LA) and CA3. In addition, propranolol treatment suppressed CREB activation by Memory retrieval. These data indicate that US-retrieval triggers more Memory traces activation than CS-retrieval does, leading to Memory Reconsolidation of more CS-US associations.
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Unconditioned- and Conditioned- Stimuli Induce Differential Memory Reconsolidation and β-AR-Dependent CREB Activation
Frontiers Media S.A., 2017Co-Authors: Bing Huang, Huiwen Zhu, Yiming Zhou, Xing LiuAbstract:Consolidated long-term fear memories become labile and reconsolidated upon retrieval by the presentation of conditioned stimulus (CS) or unconditioned stimulus (US). Whether CS-retrieval or US-retrieval will trigger different Memory Reconsolidation processes is unknown. In this study, we introduced a sequential fear conditioning paradigm in which footshock (FS) was paired with two distinct sounds (CS-A and CS-B). The treatment with propranolol, a β-adrenergic receptor (β-AR) antagonist, after US (FS)-retrieval impaired freezing behavior evoked by either CS-A or CS-B. Betaxolol, a selective β1-AR antagonist, showed similar effects. However, propranolol treatment after retrieval by one CS (e.g., CS-A) only inhibited freezing behavior evoked by the same CS (i.e., CS-A), not the other CS (CS-B). These data suggest that β-AR is critically involved in Reconsolidation of fear Memory triggered by US- and CS-retrieval, whereas β-AR blockade after US-retrieval disrupts more CS-US associations than CS-retrieval does. Furthermore, significant CREB activation in almost the whole amygdala and hippocampus was observed after US-retrieval, but CS-retrieval only stimulated CREB activation in the lateral amygdala and the CA3 of hippocampus. In addition, propranolol treatment suppressed Memory retrieval-induced CREB activation. These data indicate that US-retrieval activates more Memory traces than CS-retrieval does, leading to Memory Reconsolidation of more CS-US associations
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β arrestin biased signaling mediates Memory Reconsolidation
Proceedings of the National Academy of Sciences of the United States of America, 2015Co-Authors: Xing Liu, Bing Huang, Ye Zheng TaoAbstract:A long-standing hypothesis posits that a G protein-coupled signaling pathway mediates β-adrenergic nervous system functions, including learning and Memory. Here we report that Memory retrieval (reactivation) induces the activation of β1-adrenergic β-arrestin signaling in the brain, which stimulates ERK signaling and protein synthesis, leading to postreactivation Memory restabilization. β-Arrestin2-deficient mice exhibit impaired Memory Reconsolidation in object recognition, Morris water maze, and cocaine-conditioned place preference paradigms. Postreactivation blockade of both brain β-adrenergic Gs protein- and β-arrestin-dependent pathways disrupts Memory Reconsolidation. Unexpectedly, selective blockade of the Gs/cAMP/PKA signaling but not the β-arrestin/ERK signaling by the biased β-adrenergic ligands does not inhibit Reconsolidation. Moreover, the expression of β-arrestin2 in the entorhinal cortex of β-arrestin 2-deficient mice rescues β1-adrenergic ERK signaling and Reconsolidation in a G protein pathway-independent manner. We demonstrate that β-arrestin-biased signaling regulates Memory Reconsolidation and reveal the potential for β-arrestin-biased ligands in the treatment of Memory-related disorders.
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β-Arrestin–biased signaling mediates Memory Reconsolidation
Proceedings of the National Academy of Sciences of the United States of America, 2015Co-Authors: Xing Liu, Bing Huang, Ye Zheng TaoAbstract:A long-standing hypothesis posits that a G protein-coupled signaling pathway mediates β-adrenergic nervous system functions, including learning and Memory. Here we report that Memory retrieval (reactivation) induces the activation of β1-adrenergic β-arrestin signaling in the brain, which stimulates ERK signaling and protein synthesis, leading to postreactivation Memory restabilization. β-Arrestin2-deficient mice exhibit impaired Memory Reconsolidation in object recognition, Morris water maze, and cocaine-conditioned place preference paradigms. Postreactivation blockade of both brain β-adrenergic Gs protein- and β-arrestin-dependent pathways disrupts Memory Reconsolidation. Unexpectedly, selective blockade of the Gs/cAMP/PKA signaling but not the β-arrestin/ERK signaling by the biased β-adrenergic ligands does not inhibit Reconsolidation. Moreover, the expression of β-arrestin2 in the entorhinal cortex of β-arrestin 2-deficient mice rescues β1-adrenergic ERK signaling and Reconsolidation in a G protein pathway-independent manner. We demonstrate that β-arrestin-biased signaling regulates Memory Reconsolidation and reveal the potential for β-arrestin-biased ligands in the treatment of Memory-related disorders.
Jonathan L.c. Lee - One of the best experts on this subject based on the ideXlab platform.
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Memory Reconsolidation in aversive and appetitive settings
Frontiers in behavioral neuroscience, 2013Co-Authors: Amy C. Reichelt, Jonathan L.c. LeeAbstract:Memory Reconsolidation has been observed across species and in a number of behavioral paradigms. The majority of Memory Reconsolidation studies have been carried out in Pavlovian fear conditioning and other aversive Memory settings, with potential implications for the treatment of post-traumatic stress disorder. However, there is a growing literature on Memory Reconsolidation in appetitive reward-related Memory paradigms, including translational models of drug addiction. While there appears to be substantial similarity in the basic phenomenon and underlying mechanisms of Memory Reconsolidation across unconditioned stimulus valence, there are also notable discrepancies. These arise both when comparing aversive to appetitive paradigms and also across different paradigms within the same valence of Memory. We review the demonstration of Memory Reconsolidation across different aversive and appetitive Memory paradigms, the commonalities and differences in underlying mechanisms and the conditions under which each Memory undergoes Reconsolidation. We focus particularly on whether principles derived from the aversive literature are applicable to appetitive settings, and also whether the expanding literature in appetitive paradigms is informative for fear Memory Reconsolidation.
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Over-expectation generated in a complex appetitive goal-tracking task is capable of inducing Memory Reconsolidation
Psychopharmacology, 2013Co-Authors: Amy C. Reichelt, Jonathan L.c. LeeAbstract:Rationale Discrepancies in an expected outcome have been demonstrated to result in modification of behaviour in both appetitive and aversive conditioning settings. Objectives In this study, we sought to establish whether overexpectation generated from compound conditioning with two previously rewarded stimuli was able to induce Memory destabilisation and subsequent Reconsolidation in a Pavlovian conditioned approach setting. Results It was shown that 4 days, but not 1 day, of overexpectation training was required to induce Memory Reconsolidation, and this was disrupted by application of the NMDA subtype of glutamate receptor antagonist MK-801 prior to overexpectation training, but not by MK-801 application 6 h post-training. Conclusions These data provide evidence that the memories underlying Pavlovian conditioned approach do undergo Reconsolidation and that such Reconsolidation can be triggered by overexpectation. Therefore, the updating of appetitive conditioned stimulus and unconditioned stimulus associations underpinning conditioned responding in manners other than extinction training is likely achieved through Memory Reconsolidation.
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Mechanisms and Functions of Hippocampal Memory Reconsolidation
Memory Reconsolidation, 2013Co-Authors: Jonathan L.c. LeeAbstract:Abstract Memory Reconsolidation is the process that serves to restabilize a Memory that has been destabilized through Memory retrieval. This retrieval-induced plasticity has been extensively studied in the hippocampus, among other neural loci. A focus on hippocampal Memory Reconsolidation, for contextual fear, pure contextual, and spatial memories, reveals interesting constraints on when a retrieved Memory undergoes Reconsolidation. Moreover, the emergence of dissociable mechanisms of hippocampal contextual fear Memory consolidation and Reconsolidation has allowed the demonstration that Reconsolidation serves to update both the strength and the content of hippocampal memories. This provides compelling evidence that, at least in the hippocampus, Reconsolidation exists in order to modify memories. However, whether or not these hippocampal findings can be generalized to nonhippocampal memories remains to be determined.
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Behavioural Memory Reconsolidation of food and fear memories
Nature communications, 2011Co-Authors: Charlotte R. Flavell, David J. Barber, Jonathan L.c. LeeAbstract:Memory retrieval followed by extinction training has been shown to erase fear memories. Flavell et al. show that this approach also erases appetitive memories in rats and results from a modification of Memory Reconsolidation, which could be useful for the treatment of drug addiction.
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Memory Reconsolidation Mediates the Updating of Hippocampal Memory Content
Frontiers in behavioral neuroscience, 2010Co-Authors: Jonathan L.c. LeeAbstract:The retrieval or reactivation of a Memory places it into a labile state, requiring a process of Reconsolidation to restabilize it. This retrieval-induced plasticity is a potential mechanism for the modification of the existing Memory. Following previous data supportive of a functional role for Memory Reconsolidation in the modification of Memory strength, here I show that hippocampal Memory Reconsolidation also supports the updating of contextual Memory content. Using a procedure that separates the learning of pure context from footshock-motivated contextual fear learning, I demonstrate doubly dissociable hippocampal mechanisms of initial context learning and subsequent updating of the neutral contextual representation to incorporate the footshock. Contextual Memory consolidation was dependent upon BDNF expression in the dorsal hippocampus, whereas the footshock modification of the contextual representation required the expression of Zif268. These mechanisms match those previously shown to be selectively involved in hippocampal Memory consolidation and Reconsolidation, respectively. Moreover, Memory reactivation is a necessary step in modifying Memory content, as inhibition of hippocampal synaptic protein degradation also prevented the footshock-mediated Memory modification. Finally, dorsal hippocampal knockdown of Zif268 impaired the Reconsolidation of the pure contextual Memory only under conditions of weak context Memory training, as well as failing to disrupt contextual freezing when a strong contextual fear Memory is reactivated by further conditioning. Therefore, an adaptive function of the reactivation and Reconsolidation process is to enable the updating of Memory content.
Victor A. Molina - One of the best experts on this subject based on the ideXlab platform.
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Effect of a positive reinforcing stimulus on fear Memory Reconsolidation in ethanol withdrawn rats: Influence of d-cycloserine.
Behavioural brain research, 2016Co-Authors: Vanesa Ortiz, Victor A. Molina, Irene D. MartijenaAbstract:The pharmacological blockade of Memory Reconsolidation has been suggested as a potential treatment to the attenuation of maladaptive memories associated to psychiatric disorders and drug addiction. To interfere with the process of fear Memory Reconsolidation using a manipulation safer than pharmacological interventions, here we examined whether a positive reinforcing stimulus (non-alcoholic beer, NB) post-Memory retrieval can decrease the fear response in ethanol withdrawn (ETOH) animals. We first evaluated the potential interfering effect of NB on Memory Reconsolidation in non-ethanol dependent (control, CON) rats. Non-alcoholic beer intake shortly after Memory retrieval attenuated the fear response in CON rats. A resistance to destabilization/Reconsolidation process was previously observed in ETOH rats, which was reversed by the activation of NMDA receptor induced by pre-retrieval d-cycloserine (DCS) administration. Therefore, the influence of DCS (5mg/kg; i.p.) to facilitate the disruptive effect of NB on fear Memory was examined in ETOH animals. As expected, NB was ineffective to attenuate the fear response in ETOH rats, with DCS being necessary to promote the disruptive effect of NB on the Reconsolidation in these animals. Hence, DCS/reinforcing stimulus in combination with Memory reactivation can be considered as an alternative approach for disrupting resistant fear memories.
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The effect of Midazolam and Propranolol on fear Memory Reconsolidation in ethanol-withdrawn rats: influence of d-cycloserine.
The international journal of neuropsychopharmacology, 2015Co-Authors: Vanesa Ortiz, Victor A. Molina, Marcelo Giachero, Pablo Javier Espejo, Irene D. MartijenaAbstract:Background: Withdrawal from chronic ethanol facilitates the formation of contextual fear Memory and delays the onset to extinction, with its retrieval promoting an increase in ethanol consumption. Consequently, manipulations aimed to reduce these aversive memories, may be beneficial in the treatment of alcohol discontinuation symptoms. Related to this, pharmacological Memory Reconsolidation blockade has received greater attention due to its therapeutic potential. Methods: Here, we examined the effect of post-reactivation amnestic treatments such as Midazolam (MDZ, 3 mg/kg i.p) and Propranolol (PROP, 5 mg/kg i.p) on contextual fear Memory Reconsolidation in ethanol- withdrawn (ETOH) rats. Next, we examined whether the activation of N-methyl-D-aspartate (NMDA) receptors induced by d-cycloserine (DCS, 5 mg/kg i.p., a NMDA partial agonist) before Memory reactivation can facilitate the disruptive effect of PROP and MDZ on fear Memory in ETOH rats. Results: We observed a resistance to the disruptive effect of both MDZ and PROP following Memory reactivation. Although intra-basolateral amygdala (BLA; 1.25 ug/side) and systemic PROP administration attenuated fear Memory in DCS pre-treated ETOH rats, DCS/MDZ treatment did not affect Memory in these animals. Finally, a decrease of both total and surface protein expression of the α1 GABAA receptor (GABAA-R) subunit in BLA was found in the ETOH rats. Conclusions: Ethanol withdrawal facilitated the formation of fear Memory resistant to labilization post-reactivation. DCS administration promoted the disruptive effect of PROP on Memory Reconsolidation in ETOH rats. The resistance to MDZ’s disruptive effect on fear Memory Reconsolidation may be, at least in part, associated with changes in the GABAA-R composition induced by chronic ethanol administration/withdrawal.
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disruptive effect of midazolam on fear Memory Reconsolidation decisive influence of reactivation time span and Memory age
Neuropsychopharmacology, 2009Co-Authors: Silvia G Bustos, Héctor Maldonado, Victor A. MolinaAbstract:Disruptive Effect of Midazolam on Fear Memory Reconsolidation: Decisive Influence of Reactivation Time Span and Memory Age
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Opposite action of hippocampal CB1 receptors in Memory Reconsolidation and extinction.
Neuroscience, 2008Co-Authors: L. De Oliveira Alvares, B. Pasqualini Genro, Felipe Diehl, Victor A. Molina, Jorge Alberto QuillfeldtAbstract:Retrieval of a consolidated Memory triggers a number of processes which depend, among other factors, on the duration of the reactivation session: Reconsolidation requires a brief reactivation session, and extinction, a prolonged one. The scope of this study is to explore the potential role of the hippocampal endocannabinoid system on Reconsolidation and extinction processes. Bilateral infusion of the CB1 cannabinoid receptor antagonist, N-(piperidin-1-yl)-5-(4-iodophenyl)-1-(2, 4-dichlorophenyl)-4-methyl-1H-pyrazole-3-carboxamide (AM251) into the CA1 region of the dorsal hippocampus of Wistar rats after Memory reactivation facilitated the Reconsolidation of the contextual fear conditioning Memory. The inhibition of protein synthesis with DRB in the same brain region blocked Memory Reconsolidation. Both effects were persistent, lasting up to 7 days after the first retrieval experience. In contrast, the local infusion of anandamide blocked Memory Reconsolidation, an effect that was antagonized by the combined administration of anandamide with a subthreshold dose of a CB1 antagonist, supporting a CB1-mediated role of the hippocampal endocannabinoid system in the modulation of the Memory Reconsolidation. Local infusion of AM251 into CA1 blocked Memory extinction whereas the administration of anandamide facilitated it; however, when combined with a subthreshold concentration of the CB1 antagonist, anandamide did not affect the extinction process. The clear-cut, opposite effects observed in each situation suggest a possible role of the hippocampal endocannabinoid system as a switching mechanism deciding which processes will take place, either maintaining the original Memory (Reconsolidation) or promoting a new learning (extinction).
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Midazolam disrupts fear Memory Reconsolidation.
Neuroscience, 2006Co-Authors: Silvia G Bustos, Héctor Maldonado, Victor A. MolinaAbstract:The current research examines the influence of midazolam (MDZ) on Memory Reconsolidation using a contextual fear paradigm in rats, based on three context-shock training trials (0.7 mA, 3 s). First, we evaluate the effect of MDZ (1 mg/kg, i.p.) injected shortly after the training procedure. Second, we examined the influence of MDZ after a brief exposure (90 s) either in the training context (reactivation procedure) or in a neutral environment (no reactivation procedure) and one day later, freezing behavior was scored when rats were re-exposed to the training environment. Third, we investigate both the effect of MDZ administered at different times following reactivation on fear Memory and the persistence of such effect 10 days after reactivation. Finally, we test whether the MDZ effect could be reverted by a single weak training trial (0.2 mA, 3 s) or by the presentation of the same unconditioned stimulus in the absence of the conditioned stimulus as a reminder which proves to induce significant freezing in rats not previously trained. Results show that MDZ interferes with the formation of a contextual fear Memory only when administered after the reactivation procedure but not after the training procedure. This interference was effective up to 60 min after reactivation and not at a later time. No spontaneous recovery of freezing behavior was observed 11 days after MDZ injection which was not reverted by a weak training trial and by the unconditioned stimulus alone. All these data support the idea that stimulating GABA A receptor sites via MDZ selectively disrupts the Reconsolidation process of a contextual fear Memory.
Barry J. Everitt - One of the best experts on this subject based on the ideXlab platform.
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Enhancing cognition by affecting Memory Reconsolidation
Current Opinion in Behavioral Sciences, 2015Co-Authors: Emiliano Merlo, Amy L. Milton, Barry J. EverittAbstract:Fully consolidated associative memories can undergo a retrieval-dependent Reconsolidation process, which allows for the updating and strengthening of the original association. Limiting, or so-called boundary, conditions determine whether a particular retrieval event triggers Reconsolidation. Manipulating memories at Reconsolidation may offer an opportunity to improve cognitive capacities in humans by increasing Memory persistence, specificity and accuracy. Also, preventing the Reconsolidation of maladaptive memories that characterize some neuropsychiatric disorders, such as post-traumatic stress disorder or drug addiction may offer a novel approach to treatment. Here we review recent advances in understanding and manipulating Memory Reconsolidation in both animals and humans, and discuss the potential of such interventions in cognitive enhancement.
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The psychological and neurochemical mechanisms of drug Memory Reconsolidation: implications for the treatment of addiction
The European journal of neuroscience, 2010Co-Authors: Amy L. Milton, Barry J. EverittAbstract:Memory Reconsolidation is the process by which memories, destabilised at retrieval, require restabilisation to persist in the brain. It has been demonstrated that even old, well-established memories require Reconsolidation following retrieval; therefore, Memory Reconsolidation could potentially be exploited to disrupt, or even erase, aberrant memories that underlie psychiatric disorders, thereby providing a novel therapeutic target. Drug addiction is one such disorder; it is both chronic and relapsing, and one prominent risk factor for a relapse episode is the presentation of environmental cues that have previously been associated with drugs of abuse. This 'cue-induced relapse' can be accounted for in psychological terms by reinforcing memories of the pavlovian association between the cue and the drug, which can thus influence behaviour through at least three psychologically and neurobiologically dissociable mechanisms: conditioned reinforcement, conditioned approach and conditioned motivation. As each of these psychological processes could contribute to the resumption of drug-seeking following abstinence, it is important to develop treatments that can reduce drug-seeking re-established via influences on each or all of these pavlovian processes, in order to minimise the risk of a subsequent relapse. Investigation of the Memory Reconsolidation mechanisms of the memories underlying conditioned reinforcement, conditioned approach and conditioned motivation indicate that they depend upon different neurochemical systems, including the glutamatergic and adrenergic systems within limbic corticostriatal circuitry. We also discuss here the subsequent translation to the clinic of this preclinical work.
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appetitive Memory Reconsolidation depends upon nmda receptor mediated neurotransmission
Neurobiology of Learning and Memory, 2008Co-Authors: Jonathan L.c. Lee, Barry J. EverittAbstract:Abstract Memory persistence is a dynamic process involving the Reconsolidation of memories after their reactivation. Reconsolidation impairments have been demonstrated for many types of memories in rats, and signaling at N -methyl- d -aspartate (NMDA) receptors appears often to be a critical pharmacological mechanism. Here we investigated the Reconsolidation of appetitive pavlovian memories reinforced by natural rewards. In male Lister Hooded rats, systemic administration of the NMDA receptor antagonist (+)-5-methyl-10,11-dihydro- SH -dibenzo{ a , d }cyclohepten-5,10-imine maleate (MK-801, 0.1 mg/kg i.p.) either before or immediately following a brief Memory reactivation session abolished the subsequent acquisition of a new instrumental response with sucrose conditioned reinforcement. However, only when injected prior to Memory reactivation was MK-801 effective in disrupting the maintenance of a previously-acquired instrumental response with conditioned reinforcement. These results demonstrate that NMDA receptor-mediated signaling is required for appetitive pavlovian Memory Reconsolidation.
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Cue-Induced Cocaine Seeking and Relapse Are Reduced by Disruption of Drug Memory Reconsolidation
The Journal of neuroscience : the official journal of the Society for Neuroscience, 2006Co-Authors: Jonathan L.c. Lee, Amy L. Milton, Barry J. EverittAbstract:Long-lasting vulnerability to drug cue-induced relapse to a drug-taking habit is a major challenge to the treatment of drug addiction. Here we show that blockade of drug Memory Reconsolidation, through infusion of Zif268 antisense oligodeoxynucleotides into the basolateral amygdala shortly before reexposure to a cocaine-associated stimulus but not simply to the training context, severely impaired subsequently cue-maintained cocaine seeking under a second-order schedule of reinforcement and abolished cue-induced reinstatement of and relapse to cocaine seeking. This reduction in relapse after disrupted Memory Reconsolidation was not only seen after several hundred pairings of the stimulus with self-administered cocaine, but older, as well as recent, memories were also disrupted. Reconsolidation blockade may thus provide a potential therapeutic strategy for the prevention of relapse in drug addiction.
Bing Huang - One of the best experts on this subject based on the ideXlab platform.
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Unconditioned- and Conditioned- Stimuli Induce Differential Memory Reconsolidation and β-AR-Dependent CREB Activation.
Frontiers in neural circuits, 2017Co-Authors: Bing Huang, Huiwen Zhu, Yiming Zhou, Xing LiuAbstract:Consolidated long-term fear memories become labile and reconsolidated upon retrieval by the presentation of conditioned stimulus (CS) or unconditioned stimulus (US). Whether CS-retrieval or US-retrieval will trigger different Memory Reconsolidation processes is unknown. In this study, we introduced a sequential fear conditioning paradigm that Footshock was paired with two distinct Sounds. Propranolol, β-adrenergic receptor (β-AR) antagonist, treated after US-retrieval impaired freezing behavior evoked by CS-A and CS-B. Betaxolol, a selective β1-AR antagonist, showed the similar effects as propranolol. However, propranolol treatment after CS-retrieval only inhibited freezing behavior evoked by the same CS, i.e., CS-A (or CS-B), not the other CS. These data suggest that β-AR is critically involved in US-retrieval triggered Memory Reconsolidation of fear conditioning as CS-retrieval, and β-AR blockade after US-retrieval disrupts more CS-US associations than CS-retrieval does. Furthermore, US-retrieval induced significant CREB activation in almost the whole amygdala and hippocampus, but CS-retrieval only stimulated CREB activation in the lateral amygdala (LA) and CA3. In addition, propranolol treatment suppressed CREB activation by Memory retrieval. These data indicate that US-retrieval triggers more Memory traces activation than CS-retrieval does, leading to Memory Reconsolidation of more CS-US associations.
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Unconditioned- and Conditioned- Stimuli Induce Differential Memory Reconsolidation and β-AR-Dependent CREB Activation
Frontiers Media S.A., 2017Co-Authors: Bing Huang, Huiwen Zhu, Yiming Zhou, Xing LiuAbstract:Consolidated long-term fear memories become labile and reconsolidated upon retrieval by the presentation of conditioned stimulus (CS) or unconditioned stimulus (US). Whether CS-retrieval or US-retrieval will trigger different Memory Reconsolidation processes is unknown. In this study, we introduced a sequential fear conditioning paradigm in which footshock (FS) was paired with two distinct sounds (CS-A and CS-B). The treatment with propranolol, a β-adrenergic receptor (β-AR) antagonist, after US (FS)-retrieval impaired freezing behavior evoked by either CS-A or CS-B. Betaxolol, a selective β1-AR antagonist, showed similar effects. However, propranolol treatment after retrieval by one CS (e.g., CS-A) only inhibited freezing behavior evoked by the same CS (i.e., CS-A), not the other CS (CS-B). These data suggest that β-AR is critically involved in Reconsolidation of fear Memory triggered by US- and CS-retrieval, whereas β-AR blockade after US-retrieval disrupts more CS-US associations than CS-retrieval does. Furthermore, significant CREB activation in almost the whole amygdala and hippocampus was observed after US-retrieval, but CS-retrieval only stimulated CREB activation in the lateral amygdala and the CA3 of hippocampus. In addition, propranolol treatment suppressed Memory retrieval-induced CREB activation. These data indicate that US-retrieval activates more Memory traces than CS-retrieval does, leading to Memory Reconsolidation of more CS-US associations
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β arrestin biased signaling mediates Memory Reconsolidation
Proceedings of the National Academy of Sciences of the United States of America, 2015Co-Authors: Xing Liu, Bing Huang, Ye Zheng TaoAbstract:A long-standing hypothesis posits that a G protein-coupled signaling pathway mediates β-adrenergic nervous system functions, including learning and Memory. Here we report that Memory retrieval (reactivation) induces the activation of β1-adrenergic β-arrestin signaling in the brain, which stimulates ERK signaling and protein synthesis, leading to postreactivation Memory restabilization. β-Arrestin2-deficient mice exhibit impaired Memory Reconsolidation in object recognition, Morris water maze, and cocaine-conditioned place preference paradigms. Postreactivation blockade of both brain β-adrenergic Gs protein- and β-arrestin-dependent pathways disrupts Memory Reconsolidation. Unexpectedly, selective blockade of the Gs/cAMP/PKA signaling but not the β-arrestin/ERK signaling by the biased β-adrenergic ligands does not inhibit Reconsolidation. Moreover, the expression of β-arrestin2 in the entorhinal cortex of β-arrestin 2-deficient mice rescues β1-adrenergic ERK signaling and Reconsolidation in a G protein pathway-independent manner. We demonstrate that β-arrestin-biased signaling regulates Memory Reconsolidation and reveal the potential for β-arrestin-biased ligands in the treatment of Memory-related disorders.
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β-Arrestin–biased signaling mediates Memory Reconsolidation
Proceedings of the National Academy of Sciences of the United States of America, 2015Co-Authors: Xing Liu, Bing Huang, Ye Zheng TaoAbstract:A long-standing hypothesis posits that a G protein-coupled signaling pathway mediates β-adrenergic nervous system functions, including learning and Memory. Here we report that Memory retrieval (reactivation) induces the activation of β1-adrenergic β-arrestin signaling in the brain, which stimulates ERK signaling and protein synthesis, leading to postreactivation Memory restabilization. β-Arrestin2-deficient mice exhibit impaired Memory Reconsolidation in object recognition, Morris water maze, and cocaine-conditioned place preference paradigms. Postreactivation blockade of both brain β-adrenergic Gs protein- and β-arrestin-dependent pathways disrupts Memory Reconsolidation. Unexpectedly, selective blockade of the Gs/cAMP/PKA signaling but not the β-arrestin/ERK signaling by the biased β-adrenergic ligands does not inhibit Reconsolidation. Moreover, the expression of β-arrestin2 in the entorhinal cortex of β-arrestin 2-deficient mice rescues β1-adrenergic ERK signaling and Reconsolidation in a G protein pathway-independent manner. We demonstrate that β-arrestin-biased signaling regulates Memory Reconsolidation and reveal the potential for β-arrestin-biased ligands in the treatment of Memory-related disorders.