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The claustrum is a brain structure that remains shrouded in mystery due to the limited understanding of its cellular structure, neural pathways, functionality and physiological aspects. Significant research has unveiled connections spanning from the claustrum to the entire cortex as well as subcortical areas. This widespread connectivity has led to speculations of its role in integrating information from different brain regions, possibly contributing to processes such as attention, consciousness, learning and memory. Our working hypothesis posits that claustrum neural activity contributes to the acquisition, consolidation and reconsolidation of long-term memories in mice. We found evidence in CF-1 mice of a decline in behavioral performance in an inhibitory avoidance task due to intra-claustral administration of 2% lidocaine immediately after a training session or memory recall. Nevertheless, this does not seem to be the case for the acquisition or retrieval of this type of memory, although its neural activity is significantly increased after training, evaluated through c-Fos expression. Moreover, inhibition of the claustrum's synaptic activity appears to impair the consolidation but not acquisition or retrieval of an unconditioned memory formed in a nose-poke habituation task. [ABSTRACT FROM AUTHOR]

Abstract The claustrum is a brain structure that remains shrouded in mystery due to the limited understanding of its cellular structure, neural pathways, functionality and physiological aspects. Significant research has unveiled connections spanning from the claustrum to the entire cortex as well as subcortical areas. This widespread connectivity has led to speculations of its role in integrating information from different brain regions, possibly contributing to processes such as attention, consciousness, learning and memory. Our working hypothesis posits that claustrum neural activity contributes to the acquisition, consolidation and reconsolidation of long-term memories in mice. We found evidence in CF-1 mice of a decline in behavioral performance in an inhibitory avoidance task due to intra-claustral administration of 2% lidocaine immediately after a training session or memory recall. Nevertheless, this does not seem to be the case for the acquisition or retrieval of this type of memory, although its neural activity is significantly increased after training, evaluated through c-Fos expression. Moreover, inhibition of the claustrum’s synaptic activity appears to impair the consolidation but not acquisition or retrieval of an unconditioned memory formed in a nose-poke habituation task.

The paper describes the processes of consolidation and reconsolidation of auditory-verbal memory in patients diagnosed with Parkinson’s disease (G20, ICD-10) in comparison with cerebrovascular pathologies of a chronic and acute nature. The research objective was to identify the specifics of consolidation and reconsolidation of auditory-verbal memory in patients of this nosological group. The methods involved an experiment in F. Bartlett’s schema reconstruction, as well as methods of descriptive and comparative statistics. The experiment involved 104 people (67.5 ± 4.5, 21% male), including 30 patients with Parkinson’s disease (G20) (67.8 ± 4.8, 24% male), 34 patients diagnosed with sequelae of cerebral infarction (I69.3) (67.4 ± 4.4, 20% male), and 40 patients with other specified lesions of cerebral vessels on a model of chronic cerebral ischemia (CICI) (I67.8 67.6 ± 4.4, 24% male). All codes were indicated in accordance with ICD-10. The research revealed reliably significant features of consolidation and reconsolidation of auditoryverbal memory in Parkinson’s disease. The greatest number of differences belonged to the comparative analysis with the patients with chronic cerebral ischemia. This nosology was characterized by a greater number of distortion errors but few additions and sequence violations. In Parkinson’s disease, information underwent transformations already at the storing stage, which led to impairment of short-term and long-term memory. Distortion errors were more numerous than consistency errors, which casts doubt on the kinetic factor as the key one.

Relapse to alcohol abuse, often caused by cue-induced alcohol craving, is a major challenge in alcohol addiction treatment. Therefore, disrupting the cue-alcohol memories can suppress relapse. Upon retrieval, memories transiently destabilize before they reconsolidate in a process that requires protein synthesis. Evidence suggests that the mammalian target of rapamycin complex 1 (mTORC1), governing the translation of a subset of dendritic proteins, is crucial for memory reconsolidation. Here, we explored the involvement of two regulatory pathways of mTORC1, phosphoinositide 3-kinase (PI3K)-AKT and extracellular regulated kinase 1/2 (ERK1/2), in the reconsolidation process in a rat (Wistar) model of alcohol self-administration. We found that retrieval of alcohol memories using an odor-taste cue increased ERK1/2 activation in the amygdala, while the PI3K-AKT pathway remained unaffected. Importantly, ERK1/2 inhibition after alcohol memory retrieval impaired alcohol-memory reconsolidation and led to long-lasting relapse suppression. Attenuation of relapse was also induced by post-retrieval administration of lacosamide, an inhibitor of collapsin response mediator protein-2 (CRMP2)—a translational product of mTORC1. Together, our findings indicate the crucial role of ERK1/2 and CRMP2 in the reconsolidation of alcohol memories, with their inhibition as potential treatment targets for relapse prevention. [ABSTRACT FROM AUTHOR]

Background: The intense fear of blushing in public (erythrophobia) is part of the spectrum of social anxiety that affects between 3% and 13% of the population. This phobia can be very debilitating for those who suffer from it. It may stem from a difficult childhood marked by educational attitudes based on shame and humiliation as well as repeated traumatic experiences. Objective: The aim here is to explain in detail how the energy psychology techniques Clinical EFT (the manualized form of Emotional Freedom Techniques) and Energetic Memory Reconsolidation Therapy function in practice, as applied to "Jeanne," a young woman suffering from social anxiety and erythrophobia following a chaotic start in life. Method and setting: The therapeutic plan was drawn up on the theoretical basis of the scientific literature on energy psychology, which has produced convincing results in the treatment of trauma and anxiety. The therapy was threefold: (a) learning to manage anxiety autonomously using Clinical EFT, (b) trauma treatment using Energetic Memory Reconsolidation Therapy, and (c) psycho-education. Jeanne had a total of 15 sessions, two of which are detailed here to illustrate the work. At the start of each session, the SUD (Subjective Units of Distress) scale was used to rate the level of blushing anxiety (the scale ranges from 0 to 10, with 0 being no distress and 10 being the most imaginable). Results: The level of anxiety decreased from 9/10 to 3/10 between the first and last sessions. In addition, the number of problem situations encountered (blushing having generated negative emotions) dropped from 5 per week to 0 per week between the beginning and end of therapy. Jeanne's goal of not blushing at her wedding was achieved. She was able to experience the event without worrying about or even thinking about the anxiety. Conclusion: Psychotherapy based on energy techniques enabled me to treat Jeanne's social anxiety and erythrophobia in depth by targeting the sources while giving her access to an emotional regulation tool to use independently: Clinical EFT. [ABSTRACT FROM AUTHOR]

The gold standard of scientific medicine is using knowledge of underlying processes to shape treatment. This has previously not been possible for psychotherapy, but with the science of memory reconsolidation, requirements for change can be more precisely defined and can improve psychotherapeutic technique by focusing on three areas: the activation of maladaptive implicit learning, the provision of disconfirming information, and attention to transmission between consciousness and limbic memory. Overall, better understanding of processes helps liberate psychotherapy from rigidities dictated by set methods. [ABSTRACT FROM AUTHOR]

[Display omitted] The persistence of pathological memory is the basis of several psychiatric disorders. Memory retrieval induces "reconsolidation", a time interval during which the original memory becomes labile and destabilized. Time- and retrieval-dependent processes and memory reconsolidation are critical periods for memory interference. Modulating memory reconsolidation has received considerable research attention as a treatment protocol for several psychiatric conditions such as posttraumatic stress disorder, addiction, anxiety, and trauma-related disorders. This specific time window provides an opportunity for intervention regarding mental diseases. This article reviews the effect of modulating memory reconsolidation using behavioral-, brain stimulation-, and pharmacological-based interventions, which may help bridge the gap between intervention in laboratories and application in clinical practice. The potential advantages, limitations, challenges, and opportunities for memory reconsolidation manipulations were discussed. [ABSTRACT FROM AUTHOR]

The participation of DNA methylation processes in the mechanisms of anterograde and retrograde amnesia caused by impaired reconsolidation of conditioned food aversion memory by NMDA glutamate receptor antagonists or serotonin receptor antagonists, respectively, were studied on grape snails. Anterograde amnesia was characterized by impaired formation of long-term memory during repeated learning. Administration of a DNA methyltransferase (DNMT) inhibitor to amnestic animals resulted in accelerated formation of long-term memory during 1 day of repetitive training vs 3 days during initial training. In serotonin-dependent retrograde amnesia, repeated learning without DNMT inhibitor administration or after inhibitor injections led to the formation of long-term memory. The dynamics of memory formation was similar in both cases and did not differ from that during the initial training: the memory was formed within 3 days of training. Thus, epigenetic processes of DNA methylation are selectively involved in the mechanisms of anterograde amnesia, but do not participate in the mechanisms of retrograde amnesia. [ABSTRACT FROM AUTHOR]

Memory is the fundamental basis of human learning. Conceptual assessment and study of the memory mechanisms, its formation, consolidation and preservation at different levels of the structural and functional organization of the nervous system constitutes the necessary knowledge for solving many problems of practical and fundamental psychology. This article presents the study of memory, namely the process of its transition from a short-term to a more stable long-term form in a digital environment under the influence of the interference factor of social networks. The aim of the work is to study the influence of the social network interference factor on the processes of consolidation and reconsolidation of memory in adolescence. The total sample size was 68 adolescents aged 12–17 years. The authors conducted an experiment to achieve this goal. Its results showed that adolescents have difficulty remembering information in the form of short, successive videos in the digital space. It was found that videos that are characterized not only by visual accompaniment, but also by speech production are subject to better memorization. Under the influence of the interfering factor of social networks, adolescents faced difficulties in linking individual elements of stimuli with each other – they connected elements of one video with elements of another. According to one of the provisions of the theory of interference, information storage is characterized by the “unbinding” of representations of objects, followed by their reverse linking in an arbitrary combination during further reproduction.

Abstract: Introduction. Given the high prevalence of cerebral circulatory disorders (both acute and chronic), which are accompanied by a decrease in cognitive functions, for the most part, the effectiveness of rehabilitation and rehabilitation measures depends, among other things, on mnestic processes. The authors describe the characteristics of the memory consolidation and reconsolidation processes in patients with chronic (chronic cerebral ischemia) and acute (ischemic stroke in the circulation of the middle cerebral artery of hemispherical localization) disorders of the cerebral circulation. The study aimed to investigate the processes of consolidation and reconsolidation of memory in patients with impaired cerebral circulation (with acute and chronic cerebral ischemia). Methods. The research methods were methods of “10 words” and “Visual memory” by A. R. Luria, the experiment according to F. Bartlett’s scheme, methods of descriptive and comparative statistics. The total size of the research sample is 57 people aged 65.2 ± 2.78 years. The first group included patients with chronic cerebral ischemia – 21 people; the second group included the patients with left-sided localization of the ischemic stroke focus – 17 people; the third group also included patients who had suffered an ischemic stroke, 19 people – with the localization of the dextrocerebral affected area. Results. In patients with cerebral circulatory disorders, a decrease in short-term audio-verbal and visual-picturesque memory volume was revealed, regardless of the type of cerebral circulatory disorder (acute or chronic cerebral ischemia). In an ischemic stroke of hemispheric localization, a change in the qualitative and quantitative characteristics of the memory consolidation and reconsolidation processes has been experimentally proven. This change is a consequence of a decrease in the volume of short-term audio-verbal and visual-picturesque memory. Discussion. The decrease in volume leads to instability of the memory traces, which distorts the consolidated information. In the process of reconsolidation, there is a reduction (in case of chronic cerebral ischemia) and distortion (in case of ischemic stroke of hemispheric localization) of the reproduced information.

Addiction is a persistent, recurring condition characterized by repeated relapses despite the desire to control drug use or maintain sobriety. The attainment of abstinence is hindered by persistent maladaptive drug-associated memories, which drive drug-seeking and use behavior. This article examines the preliminary evidence supporting the combination of non-invasive brain stimulation (NIBS) techniques and memory editing (or reconsolidation) interventions as add-on forms of treatment for individuals with substance-related disorders (SUD). Studies have shown that NIBS can modestly reduce drug use and craving through improved cognitive control or other undetermined reasons. Memory reconsolidation, a process by which a previously consolidated memory trace can be made labile again, can potentially erase or significantly weaken SUD memories underpinning craving and the propensity for relapse. This approach conveys enthusiasm while also emphasizing the importance of managing boundary conditions and null results for interventions found on fear memory reconsolidation. Recent studies, which align with the state-dependency and activity-selectivity hypotheses, have shown that the combination of NIBS and behavioral interventions holds promise for treating SUD by reducing self-reported and physiological aspects of craving. Effective long-term outcomes for this procedure require better identification of critical memories, a deeper understanding of the brain mechanisms underlying SUD and memory reconsolidation and overcoming any boundary conditions of destabilized memories. This will enable the procedure to be personalized to the unique needs of individual patients. [ABSTRACT FROM AUTHOR]

Re-exposure to elements of prior experiences can create opportunities for inducing amnesia for those events. The dominant theoretical framework posits that such re-exposure can result in memory destabilization, making the memory representation temporarily sensitive to disruption while it awaits reconsolidation. If true, such a mechanism that allows for memories to be permanently changed could have important implications for the treatment of several forms of psychopathology. However, there have been contradictory findings and elusive occurrences of replication failures within the "reconsolidation" field. Considering its potential relevance for clinical applications, the fact that this "hot" research area is being dominated by a single mechanistic theory, and the presence of unexplainable contradictory findings, we believe that it is both useful and timely to critically evaluate the reconsolidation framework. We discuss potential issues that may arise from how reconsolidation interference has typically been deducted from behavioral observations, and provide a principled assessment of reconsolidation theory that illustrates that the theory and its proposed boundary conditions are vaguely defined, which has made it close to impossible to refute reconsolidation theory. We advocate for caution, encouraging researchers not to blindly assume that a reconsolidation process must underlie their findings, and pointing out the risks of doing so. Finally, we suggest concrete theoretical and methodological advances that can promote a fruitful translation of reminder-dependent amnesia into clinical treatment. [ABSTRACT FROM AUTHOR]

The study of neural plasticity and related memory functions is one of the fundamental fields in anesthesiology. Understanding this issue is very important both for the physician - the anesthesiologist-resuscitator, and for the patient. This review of the literature describes structures and processes of the central nervous system which in a sense are the target for the amnestic action of sedation and anesthesia medications. The possibilities of implicit and explicit memory formation depending on different levels of sedation and anesthesia are considered. Special attention is paid to the mechanism of action of GABAergic drugs on the processes of memory consolidation and reconsolidation.

Addiction is a persistent, recurring condition characterized by repeated relapses despite the desire to control drug use or maintain sobriety. The attainment of abstinence is hindered by persistent maladaptive drug-associated memories, which drive drug-seeking and use behavior. This article examines the preliminary evidence supporting the combination of non-invasive brain stimulation (NIBS) techniques and memory editing (or reconsolidation) interventions as add-on forms of treatment for individuals with substance-related disorders (SUD). Studies have shown that NIBS can modestly reduce drug use and craving through improved cognitive control or other undetermined reasons. Memory reconsolidation, a process by which a previously consolidated memory trace can be made labile again, can potentially erase or significantly weaken SUD memories underpinning craving and the propensity for relapse. This approach conveys enthusiasm while also emphasizing the importance of managing boundary conditions and null results for interventions found on fear memory reconsolidation. Recent studies, which align with the state-dependency and activity-selectivity hypotheses, have shown that the combination of NIBS and behavioral interventions holds promise for treating SUD by reducing self-reported and physiological aspects of craving. Effective long-term outcomes for this procedure require better identification of critical memories, a deeper understanding of the brain mechanisms underlying SUD and memory reconsolidation and overcoming any boundary conditions of destabilized memories. This will enable the procedure to be personalized to the unique needs of individual patients.

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Copyright of Praxis der Kinderpsychologie und Kinderpsychiatrie is the property of Vandenhoeck & Ruprecht GmbH & Co. KG and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Experiments demonstrating post-reactivation amnesia for learned fear in animals have generated a novel and influential hypothesis on the plasticity of memory, usually referred to as memory reconsolidation. The clinical potential of pharmacologically disrupting the process of memory reconsolidation has sparked a wave of interest into whether this phenomenon can also be demonstrated in humans, and ultimately harnessed for therapeutic purposes. In this essay we outline how the work of Karim Nader and colleagues has moved the field forward from a focus on extinction learning to the prospect of disrupting memory reconsolidation. We then review some promising findings on the necessary conditions, as well as potential boundary conditions, of pharmacologically disrupting the process of memory reconsolidation obtained in our laboratory. Even though laboratory experiments in animals and humans suggest that we may be at the brink of a breakthrough in fundamentally changing emotional memories, the necessary and sufficient conditions for targeting and disrupting memory reconsolidation in clinical practice are largely unknown. There is likely no universally effective reactivation procedure for triggering the reconsolidation of clinically significant emotional memories, and the impact of subtle boundary conditions observed in basic experiments compounds this issue. Notwithstanding these challenges, the discovery of changing emotional memory through disrupting the process of memory reconsolidation has unquestionably invigorated the field. [ABSTRACT FROM AUTHOR]

Scholarship has not so far raised the question whether the so-called Buddhist noble truths are actually true. The present article addresses this question in light of recent developments in neuroscience and psychology. It bases itself primarily on the theory proposed in some publications by Mark Solms, and on some other recent discoveries in psychology. Concentrating on the role of memories in the formation of personality, it draws attention to the potential effects of memory reconsolidation on those memories and shows how cessation of suffering and cessation of desire make sense in this context. Access to the relevant memories presents itself as a little understood process. Proposals are made as to how it may be attained. [ABSTRACT FROM AUTHOR]

The primary purpose of this article is to introduce emotion-based interventions to clinicians that may not be familiar with such techniques. The article explains how emotion-based interventions could help transform the effectiveness of psychotherapy beyond that of traditional interventions alone, which are associated with cognitive behavioral or psychodynamic psychotherapy. Research suggests that techniques of emotional awareness, emotional validation, self-compassion, understanding the origin of emotions, forgiveness, grief work, and memory reconsolidation could offer novel interventions to improve therapeutic outcomes. A clinical example of panic disorder is provided to demonstrate how emotional interventions would be distinguished for traditional cognitive and behavioral interventions. Clinicians are encouraged to integrate emotional interventions in conjunction with cognitive and behavioral techniques that they may already currently be familiar with to optimize their clinical practice. [ABSTRACT FROM AUTHOR]

Current theoretical models of emotional processing rely mainly on detecting emotional processing through verbal, conscious, and cognitive processes. However, artmaking can potentially reveal embodied and implicit processes that may otherwise remain hidden in verbal expression. This paper attempts to close the scholarly gap by introducing a novel art-based emotional processing model that integrates emotional processing and art therapy literature, incorporating emotional meaning-making, awareness, acceptance, and memory consolidation. The art-based EP model explains the processes through which art creation may benefit emotional processing. It also elucidates the ways in which art therapy can be used to enhance therapeutic outcomes. • The proposed novel art-based emotional processing (EP) model closes a theory gap. • The model explains how art creation benefits EP. • Two art therapy cycles promote EP, by physical interaction with art materials. • Cycle 1 helps make sense of emotions and change dysfunctional EP patterns. • Cycle 2 helps memory reconsolidation for verbal/visual expression. [ABSTRACT FROM AUTHOR]

Objective: Individuals with bulimia nervosa (BN) have a high comorbidity with posttraumatic stress disorder (PTSD), complex posttraumatic stress disorder (cPTSD) or borderline personality disorder (BPD). This case series describes the proof of concept of a novel integrative psychotherapy for adults with comorbid BN and psychological trauma. Memory reconsolidation therapy (MRT) was developed as an evolution of classic prolonged exposure therapy. The aim of this study was an initial assessment of MRT for comorbid BN and psychological trauma in a case series study. Method: MRT was used in this study to reduce trauma symptoms which may maintain disordered eating behaviour. Two women with BN and PTSD, and an additional participant with comorbid BN and BPD/cPTSD, were offered 16 weekly sessions of MRT following baseline measures. Results: At 3-month follow-up, all participants experienced a decrease in trauma symptoms as measured by the Impact of Event Scale–Revised. All participants also experienced a decrease in the frequency of self-reported BN behaviour. Conclusions: In this case series patients with BN and PTSD/cPTSD/BPD showed improvement of BN and trauma symptoms. These results offer preliminary support for the inclusion of MRT for the treatment of psychological trauma in adults with BN. KEY POINTS What is already known about this topic: There is a high prevalence rate of comorbid bulimia nervosa and posttraumatic stress disorder. Engagement in disordered eating behaviours can be a maladaptive coping strategy in response to traumatic experiences. Preliminary studies support the efficacy of memory reconsolidation therapy in treating traumatic memories. What this topic adds: (1) The results provide preliminary evidence that memory reconsolidation therapy is efficacious in reducing trauma symptoms in adults with bulimia nervosa and comorbid PTSD/cPTSD. (2) The reduction in bulimia nervosa symptoms appeared to coincide with the reduction in trauma symptoms. (3) Treating posttraumatic stress disorder symptoms in patients with comorbid bulimia nervosa and posttraumatic stress disorder has the potential to reduce both trauma symptoms and the frequency of self-reported disordered eating behaviour. [ABSTRACT FROM AUTHOR]

The participation of DNA methylation and histone acetylation in the mechanisms of anterograde amnesia and memory recovery was studied on grape snails trained in conditioned food aversion. Anterograde amnesia developed 10 days after memory reconsolidation impairment with an NMDA glutamate receptor antagonist and was characterized by long-term memory formation impairment upon repeated training. DNA methyltransferase inhibitor injections to snails 1 h before repeated training, as well as 15 min or 4 h after repeated training, caused rapid formation of memory that persisted for at least 10 days. Injections of histone deacetylase inhibitor before repeated training also induced the formation of a stable long-term memory. However, administration of histone deacetylase inhibitor 15 min after repeated training initiated a temporary memory recovery. Injections of the inhibitor 4 h after repeated training were ineffective. These results indicate that histone-dependent chromatin remodeling and DNA methylation are selectively involved in the mechanisms of anterograde amnesia and memory recovery. [ABSTRACT FROM AUTHOR]

Introduction: In recent years, yoga has been used as an intervention to improve memory function. The present study aims to investigate the effect of super-brain yoga practices on the consolidation and reconsolidation of motor memory in young girls. Materials and Methods: Participants were 24 young girls in Lendeh, selected based on the inclusion criteria of the study and then randomly divided into two groups: experimental group (performing ten blocks of 80 trials in the acquisition phase, performing super brain yoga, recalling the tasks after 15 minutes and performing the retention test after one hour) and the control group (performing ten blocks of 80 trials in the acquisition phase, recalling the tasks after 14 days from the last training block of the acquisition phase and performing the retention test after one hour). Data was collected using the Altering Serial Reaction Time Task. Results: The results of variance analysis with the repeated measure in acquiring phase demonstrated that the subjects’ performance improved during the training trials (P<0.05) and the subjects had a better performance in the ninth and tenth training blocks than in the first. In the first retention test, both the super brain yoga group and control group made progress (P<0.05), however, the super brain yoga group made more progress than the latter. In the second memory test, the yoga practice group performed better than in the first retention test and the tenth training block. Conclusion: Remarkably, the results of the study show that applying the intervention super brain yoga not only led to memory inhibition but also acted as a facilitator for consolidating and reconsolidating motor memory [ABSTRACT FROM AUTHOR]

This publication presents the qualitative findings from a mixed-method pilot study on three- and four-drawing protocols for chronic pain, which have demonstrated significant positive quantitative results. For this report, thematic analysis and magnitude coding of drawing titles, narratives, and characteristics including resource representations and integration, was conducted. Findings demonstrated positive changes associated with specific drawing protocol prompts and sequences. Participants (N = 25) reported positive changes, demonstrated in part by their final drawings, which integrated depictions of their resources. Findings included positive shifts in cognitive and affective functioning, social support, stress levels, psychological processing, pain experiences, and representations of self. These findings suggested further support for the clinical utility of drawing protocols for chronic pain. [ABSTRACT FROM AUTHOR]

Memory destabilization and reconsolidation is hypothesized to be a fundamental mnemonic process that can underpin memory updating. Instrumental memories have been shown recently to be destabilized following a reactivation session that involves a change in instrumental reward contingency. However, the acquisition and performance of an instrumental response occurs in the presence of the learning of other reward-related memories. This may influence the ability of a given reactivation session to destabilize the previously learned instrumental memory. Here we present a series of experiments in male rats involving an instrumental memory trained on an FR1 schedule over 10 days, and then reactivated in a session that imposed a VR5 schedule of reinforcement. When MK-801 was injected prior to the VR5 reactivation session, it reliably impaired subsequent instrumental performance at test only when the reactivation session occurred 48 h, and not 24 h, after the end of training. The interposition between the end of training and the reactivation session of a context extinction session, an additional VR5 reactivation session, or indeed the simple experience of being handled and injected with vehicle, resulted in MK-801 no longer having an amnestic effect on test performance. While we do not have a clear account for the process and mechanism underpinning this apparent selectivity of the effect of the VR5 session to destabilize the instrumental memory, it does additionally highlight the need for greater understanding of the conditions that facilitate reactivation-induced memory destabilization. [ABSTRACT FROM AUTHOR]

Individual differences in the ability to habitually regulate emotion may impact the efficacy of fear memory extinction. The aim of this study was to assess the relationship between dispositional cognitive reappraisal and expressive suppression with post-retrieval and standard extinction. Fear memory and extinction were measured with the recovery of skin conductance responses. We also examined the relationship between a temporal feature of electrodermal responding (half recovery time) and each of the emotion regulation strategies. University students (N = 80) underwent a three-day fear conditioning procedure using a within subject design consisting of acquisition on day one, post-retrieval extinction and standard extinction on day two, and recovery test on day three. Individual difference data on self-reported levels of cognitive reappraisal, expressive suppression, trait anxiety, and depression were collected. We did not detect a relationship between the two emotion regulation strategies measured in this study and acquisition or extinction. We found, however, that increased dispositional use of cognitive reappraisal was associated with lower spontaneous recovery to both the post-retrieval extinction and standard extinction stimulus after controlling for age, trait anxiety, and depression. There were no associations between expressive suppression and conditioned responses. We also observed patterns of faster dissipation of arousal for reappraisal and slower for suppression to the conditioned stimulus during extinction training, which may represent the unique influence of each emotion strategy on the regulation of fear. We conclude greater daily use of cognitive reappraisal, but not expressive suppression, associates with extinction retention after receiving both standard and post-retrieval extinction. [ABSTRACT FROM AUTHOR]

Memory destabilization and reconsolidation is hypothesized to be a fundamental mnemonic process that can underpin memory updating. Instrumental memories have been shown recently to be destabilized following a reactivation session that involves a change in instrumental reward contingency. However, the acquisition and performance of an instrumental response occurs in the presence of the learning of other reward-related memories. This may influence the ability of a given reactivation session to destabilize the previously learned instrumental memory. Here we present a series of experiments in male rats involving an instrumental memory trained on an FR1 schedule over 10 days, and then reactivated in a session that imposed a VR5 schedule of reinforcement. When MK-801 was injected prior to the VR5 reactivation session, it reliably impaired subsequent instrumental performance at test only when the reactivation session occurred 48 h, and not 24 h, after the end of training. The interposition between the end of training and the reactivation session of a context extinction session, an additional VR5 reactivation session, or indeed the simple experience of being handled and injected with vehicle, resulted in MK-801 no longer having an amnestic effect on test performance. While we do not have a clear account for the process and mechanism underpinning this apparent selectivity of the effect of the VR5 session to destabilize the instrumental memory, it does additionally highlight the need for greater understanding of the conditions that facilitate reactivation-induced memory destabilization.

Post-reactivation amnesia of contextual fear memories by blockade of noradrenergic signaling has been shown to have limited replicability in rodents. This is usually attributed to several boundary conditions that gate the destabilization of memory during its retrieval. How these boundary conditions can be overcome, and what neural mechanisms underlie post-reactivation changes in contextual fear memories remain largely unknown. Here, we report a series of experiments in a contextual fear-conditioning paradigm in mice, that were aimed at solving these issues. We first attempted to obtain a training paradigm that would consistently result in contextual fear memory that could be destabilized upon reactivation, enabling post-retrieval amnesia by the administration of propranolol. Unexpectedly, our attempts were unsuccessful to this end. Specifically, over a series of experiments in which we varied different parameters of the fear acquisition procedure, at best small and inconsistent effects were observed. Additionally, we found that propranolol did not alter retrieval-induced neural activity, as measured by the number of c-Fos+ cells in the hippocampal dentate gyrus. To determine whether propranolol was perhaps ineffective in interfering with reactivated contextual fear memories, we also included anisomycin (i.e., a potent and well-known amnesic drug) in several experiments, and measures of synaptic glutamate receptor subunit GluA2 (i.e., a marker of memory destabilization). No post-retrieval amnesia by anisomycin and no altered GluA2 expression by reactivation was observed, suggesting that the memories did not undergo destabilization. The null findings are surprising, given that the training paradigms we implemented were previously shown to result in memories that could be modified upon reactivation. Together, our observations illustrate the elusive nature of reactivation-dependent changes in non-human fear memory. [ABSTRACT FROM AUTHOR]

The role of autobiographical memory is not just to relate us to our past self, but also to shape the future self of ours by helping us navigate the complex world we encounter in our every-day lives on a stable basis: some more or less vivid idea of who we really are as persons, as individual beings with distinct selves and unique identities. In this sense memory has also to do with being and becoming, and not just with having been. The advances in the field of memory neuroscience have resulted in what is called memory reconsolidation, that is, techniques to suppress, modify, or enhance certain memories that have to do with our moral identity and moral status. In this presentation I will discuss certain potential implications of memory reconsolidation that are in my view of key importance for neuroethics, and especially for the debate concerning moral identity, agency and status in the brand-new landscape that has been shaped by the novel capabilities neuroscience has made available. [ABSTRACT FROM AUTHOR]

Abstract—The current review provides data on the association between neuroinflammation and reconsolidation of memory. The first part of the review gives the general characteristics of the phenomenon of reconsolidation and the use of the destabilization phase of memory for its subsequent modifications to erase a negative memory. We also describe the role of the immune system (microglia and astrocytes) in the formation of neuroinflammation and the participation of the proinflammatory agents in diseases associated with cognitive disorders (Alzheimer's and Parkinson's diseases). In the next section, we discuss the influence of neuroinflammation on behavioral manifestations of negative memory reconsolidation, molecular-cellular mechanisms, and signaling pathways involved in its impairment under the influence of proinflammatory cytokines. We also describe the modulatory influence of neuroinflammation on the reconsolidation of positive memory (associated with drug use) on models of self-administration of drugs and conditioned place preference with concomitant molecular-cellular mechanisms and structures involved that are associated with the reinforcing properties of drugs. [ABSTRACT FROM AUTHOR]

Post-reactivation amnesia of contextual fear memories by blockade of noradrenergic signaling has been shown to have limited replicability in rodents. This is usually attributed to several boundary conditions that gate the destabilization of memory during its retrieval. How these boundary conditions can be overcome, and what neural mechanisms underlie post-reactivation changes in contextual fear memories remain largely unknown. Here, we report a series of experiments in a contextual fear-conditioning paradigm in mice, that were aimed at solving these issues. We first attempted to obtain a training paradigm that would consistently result in contextual fear memory that could be destabilized upon reactivation, enabling post-retrieval amnesia by the administration of propranolol. Unexpectedly, our attempts were unsuccessful to this end. Specifically, over a series of experiments in which we varied different parameters of the fear acquisition procedure, at best small and inconsistent effects were observed. Additionally, we found that propranolol did not alter retrieval-induced neural activity, as measured by the number of c-Fos+ cells in the hippocampal dentate gyrus. To determine whether propranolol was perhaps ineffective in interfering with reactivated contextual fear memories, we also included anisomycin (i.e., a potent and well-known amnesic drug) in several experiments, and measures of synaptic glutamate receptor subunit GluA2 (i.e., a marker of memory destabilization). No post-retrieval amnesia by anisomycin and no altered GluA2 expression by reactivation was observed, suggesting that the memories did not undergo destabilization. The null findings are surprising, given that the training paradigms we implemented were previously shown to result in memories that could be modified upon reactivation. Together, our observations illustrate the elusive nature of reactivation-dependent changes in non-human fear memory.

Abstract Memory reconsolidation is thought to maintain or enhance an original memory or add new information to the memory. Retrieved inhibitory avoidance (IA) memory is enhanced through memory reconsolidation by activating gene expression in the amygdala, medial prefrontal cortex (mPFC), and hippocampus. However, it remains unclear how these regions interact to reconsolidate/enhance IA memory. Here, we found the interactions between the amygdala and mPFC as upstream regulators of the hippocampus for IA memory reconsolidation. Pharmacological inactivation of the amygdala, mPFC, or hippocampus immediately after IA memory retrieval blocked IA memory enhancement. More importantly, inactivation of the amygdala or mPFC blocked the induction of c-Fos in the amygdala, mPFC, and hippocampus, whereas hippocampal blockade inhibited it only in the hippocampus. These observations suggest interactions between the amygdala and mPFC and they both function as upstream regulators of the hippocampus to reconsolidate IA memory. Our findings suggest circuitry mechanisms underlying IA memory enhancement through reconsolidation between the amygdala, mPFC, and hippocampus.

The research on memory reconsolidation, in neuroscientific field, want to dimostrate that is possibile the cancellation of “emotion learning” reported in implicit memory. This paper want to examine some of these results and how they can be traslate in therapeutic practice, in order to provide a common change’s model and empirically confirmed. This new trans- theoretical knowledge, entrusted to clinic professionals, could have an impact, both on psycotherapy’s effectiveness, and on models of psychological treatment. This work try to explain the memory reconsolidation process and underline that this process is responsable of changing therapy. This evidence is different from other changing’s models actually dominat in clinic paradigm that aspire to “autoregolation”.

Through classical conditioning procedure, subjects give the conditioned response to the neutral stimuli (to which at the beginning no response was elicited) as a result of its pairing with the unconditioned stimuli. To reverse this procedure, extinction paradigm is performed. Several problems might arise as a result of the extinction process that are renewal, reinstatement, and spontaneous recovery of the conditioned response. However, memory reconsolidation view seems to offer considerable solutions to those problems. Accordingly, acquired memories do not stay in their consolidated and stable state. Instead, every time they are reactivated, they become labile and then reconsolidated again with the subsequent protein synthesis. Thus, interventions during this labile state would offer modifications in the original memory, meaning that they could also provide a solution to the problems arisen as a result of extinction procedure. In the light of the neuropsychoanalytic literature, the current review examined whether or not the technique of free association would lead to the reactivation of original memories while rendering them labile which might also result in modifications in them. [ABSTRACT FROM AUTHOR]

Objective: Researchers have suggested that psychotherapy may be enhanced by the addition of 3,4‐methylenedioxymethamphetamine (MDMA), particularly in the treatment of disorders wherein interpersonal dysfunction is central, such as social anxiety disorder. We review literature pertaining to three potential processes of change that may be instigated during sessions involving MDMA administration in the treatment of social anxiety disorder. Design: This is a narrative review that integrates research on the etiology and maintenance of social anxiety disorder and mechanisms of action of MDMA to examine how MDMA may enhance psychotherapy outcomes. Results: We first outline how MDMA may enhance memory reconsolidation in social anxiety disorder. We then discuss how MDMA may induce experiences of self‐transcendence and self‐transcendent emotions such as compassion, love, and awe; and how these experiences may be therapeutic in the context of social anxiety disorder. We subsequently discuss the possibility that MDMA may enhance the strength and effectiveness of the therapeutic relationship which is a robust predictor of outcomes across many disorders as well as a potential key ingredient in treating disorders where shame and social disconnection are central factors. Conclusion: We discuss how processes of change may extend beyond the MDMA dosing sessions themselves. [ABSTRACT FROM AUTHOR]

Studies with cannabidiol (CBD) suggest that this compound has anxiolytic properties and may mediate the reconsolidation and extinction of aversive memories. The objective of this study was to test whether the administration of CBD 300 mg before the recall of traumatic events attenuated symptoms usually induced by recall in subjects diagnosed with posttraumatic stress disorder (PTSD) and if its potential effects interfere with the reconsolidation of aversive memories. The double-blind trial included 33 participants of both sexes, aged between 18 and 60 years, diagnosed with PTSD according to the SCID-5 and randomly allocated to two groups treated with CBD (n = 17) and placebo (n = 16). In the first experimental section, participants were matched by sex, age, body mass index (BMI), and PTSD symptoms as assessed with the Posttraumatic Stress Disorder Checklist (PCL-5). On the same day, participants prepared the behavior test, recording accounts of their traumas in digital audio for a minute and a half and then imagining the trauma for 30 s. After 7 days, participants received CBD (300 mg) or placebo and performed the behavioral test, listening to the trauma account and imagining themselves in that situation. Before and after the behavioral test, subjective changes in mood and anxiety were recorded (Visual and Analogical Mood Scale — VAMS and STAI-state), along with physiological correlates of anxiety blood pressure (BP), heart rate (HR), and salivary cortisol (SC). Seven days later, participants underwent the same procedures as the previous session, but without the pharmacological intervention, to assess the effect on reconsolidation of traumatic memories. We found that CBD significantly attenuated the increase in the VAMS scale cognitive impairment factor scores, under the CBD's effect, with this effect remaining 1 week after drug administration. No significant differences between the effects of CBD and placebo on anxiety, alertness, and discomfort induced by the recall of the traumatic event during the pharmacological intervention and in the subsequent week, in the absence of it. There were no significant differences between the CBD and placebo groups regarding physiological data (BP, HR, and SC). The attenuation of cognitive impairments during trauma recall under the effect of CBD may have interfered with the reconsolidation of traumatic memories concerning its association with cognitive impairments. [ABSTRACT FROM AUTHOR]

Background: Intrusive memories (IMs) of traumatic events are a key symptom of posttraumatic stress disorder (PTSD), and contribute to its maintenance. This translational proof-of-principle study tested whether a single-session behavioural intervention reduced the number of childbirth-related IMs (CB-IMs) and childbirth-related PTSD (CB-PTSD) symptoms, in women traumatised by childbirth. The intervention was assumed to disrupt trauma memory reconsolidation.Methods: In this pre-post study, 18 participants, whose traumatic childbirth had occurred between seven months and 6.9 years before, received an intervention combining childbirth-related reminder cues (including the return to maternity unit) with a visuospatial task. They recorded their daily CB-IMs in the two weeks pre-intervention (diary 1), the two weeks post-intervention (diary 2; primary outcome), and in week 5 and 6 post-intervention (diary 3). CB-PTSD symptom severity was assessed five days pre-intervention and one month post-intervention.Results: Compared to diary 1, 15/18 participants had ≥ 50% fewer CB-IMs in diary 2. The median (IQR) reduction of the number of CB-IMs was 81.89% (39.58%) in diary 2, and persisted in diary 3 (n = 17). At one month post-intervention, CB-PTSD symptom severity was reduced by ≥ 50% in 10/18 participants. Of the 8 participants with a CB-PTSD diagnosis pre-intervention, none met diagnostic criteria post-intervention. The intervention was rated as highly acceptable.Limitations: The design limits the causal interpretation of observed improvements.Conclusion: This is the first time such a single-session behavioural intervention was tested for old and real-life single-event trauma. The promising results justify a randomized controlled trial, and may be a first step toward an innovative CB-PTSD treatment. [ABSTRACT FROM AUTHOR]

Impairment of reconsolidation of conditioned food aversion memory led to the development of a specific anterograde amnesia: repeated training of amnestic snails did not induce long-term memory formation. DNA demethylation caused by injections of DNA methyltransferase inhibitor (DNAMT) during repeated training led to long-term memory formation. Injections of an NMDA glutamate receptor antagonist or a serotonin receptor antagonist prevented memory formation induced by administration of DNAMT inhibitor and repeated training. We hypothesize that methylation-dependent repression of neuronal genes underlies anterograde amnesia. Demethylation eliminated the blockade of these genes and created conditions for long-term memory formation, the induction mechanisms of which involve neurotransmitter receptors. [ABSTRACT FROM AUTHOR]

This article describes memory reconsolidation and how the author uses the concept to explain the success of a psychotherapy session using eye movement desensitization and reprocessing (EMDR). A transcript of the session is provided to demonstrate how the author works in a relational way and to give a personal example of how memory reconsolidation occurs in everyday life. [ABSTRACT FROM AUTHOR]

Abstract Background Posttraumatic stress disorder (PTSD) may stem from the formation of aberrant and enduring aversive memories. Some PTSD patients have recreationally used Cannabis, probably aiming at relieving their symptomatology. However, it is still largely unknown whether and how Cannabis or its psychotomimetic compound Δ9-tetrahydrocannabinol (THC) attenuates the aversive/traumatic memory outcomes. Here, we seek to review and discuss the effects of THC on aversive memory extinction and anxiety in healthy humans and PTSD patients. Methods Medline, PubMed, Cochrane Library, and Central Register for Controlled Trials databases were searched to identify peer-reviewed published studies and randomized controlled trials in humans published in English between 1974 and July 2020, including those using only THC and THC combined with cannabidiol (CBD). The effect size of the experimental intervention under investigation was calculated. Results At low doses, THC can enhance the extinction rate and reduce anxiety responses. Both effects involve the activation of cannabinoid type-1 receptors in discrete components of the corticolimbic circuitry, which could couterbalance the low “endocannabinoid tonus” reported in PTSD patients. The advantage of associating CBD with THC to attenuate anxiety while minimizing the potential psychotic or anxiogenic effect produced by high doses of THC has been reported. The effects of THC either alone or combined with CBD on aversive memory reconsolidation, however, are still unknown. Conclusions Current evidence from healthy humans and PTSD patients supports the THC value to suppress anxiety and aversive memory expression without producing significant adverse effects if used in low doses or when associated with CBD. Future studies are guaranteed to address open questions related to their dose ratios, administration routes, pharmacokinetic interactions, sex-dependent differences, and prolonged efficacy.

Scholarship has not so far raised the question whether the so-called Buddhist noble truths are actually true. The present article addresses this question in light of recent developments in neuroscience and psychology. It bases itself primarily on the theory proposed in some publications by Mark Solms, and on some other recent discoveries in psychology. Concentrating on the role of memories in the formation of personality, it draws attention to the potential effects of memory reconsolidation on those memories and shows how cessation of suffering and cessation of desire make sense in this context. Access to the relevant memories presents itself as a little understood process. Proposals are made as to how it may be attained.

Maladaptive emotional memories are a transdiagnostic feature of mental health problems. Therefore, understanding whether and how emotional memories can change might help to prevent and treat mental disorders. We tested whether neutral memories of naturalistic events can retroactively acquire positive or negative affect, in a preregistered three-day Modification of Valence in Episodes (MOVIE) paradigm. On Day 1, participants (N = 41) encoded memories of neutral movie scenes, representing lifelike naturalistic experiences. On Day 2, they retrieved each episode before viewing a happy, sad, or neutral scene from the same movie (yielding a within-subjects design with a neutral-negative, neutral-positive, and neutral-neutral condition). On Day 3, participants again retrieved each memory from Day 1. We assessed the affective tone of episodes through facial expressions of positive and negative affect (using facial electromyography, fEMG) and through self-reported feelings. Positive updating of neutral episodes led to increased expressions of positive affect, whereas negative updating led to increased self-reported negative feelings. These results suggest that complex neutral episodic memories can retroactively acquire an affective tone, but the effects were modest and inconsistent across affect readouts. Future research should investigate alternative approaches to updating emotional memories that produce more profound changes in the valence of memories., Competing Interests: Declaration of competing interest None., (Copyright © 2024 The Authors. Published by Elsevier Ltd.. All rights reserved.)