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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]

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]

Relapse to alcohol abuse is often caused by exposure to potent alcohol-associated cues. Therefore, disruption of the cue-alcohol memory can prevent relapse. It is believed that memories destabilize and become prone for updating upon their reactivation through retrieval and then restabilize within 6 h during a "reconsolidation" process. We recently showed that relapse to cocaine seeking in a place-conditioning paradigm could be prevented by counterconditioning the cocaine cues with aversive outcomes following cocaine-memory retrieval. However, to better model addiction-related behaviors, self-administration models are necessary. Here, we demonstrate that relapse to alcohol seeking can be prevented by aversive counterconditioning conducted during alcohol-memory reconsolidation, in the place conditioning and operant self-administration paradigms, in mice and rats, respectively. We found that the reinstatement of alcohol-conditioned place preference was abolished only when aversive counterconditioning with water flooding was given shortly after alcohol-memory retrieval. Furthermore, rats trained to lever press for alcohol showed decreased context-induced renewal of alcohol-seeking responding when the lever pressing was punished with foot-shocks, shortly, but not 6 h, after memory retrieval. These results suggest that aversive counterconditioning can prevent relapse to alcohol seeking only when performed during alcohol-memory reconsolidation, presumably by updating, or replacing, the alcohol memory with aversive information. Finally, we found that aversive counterconditioning preceded by alcohol-memory retrieval was characterized by the upregulation of brain-derived neurotrophic factor (Bdnf) mRNA expression in the medial prefrontal cortex, suggesting that BDNF may play a role in the memory updating process. [ABSTRACT FROM AUTHOR]

Within our civilian population, Intimate Partner Violence (IPV) has become a major health problem. Consequences of anger and aggression have resulted in incarceration rates which place the United States as the world's leader with 2.2 million people in prisons and jails. The current treatment of anger and aggression is based primarily on theories that were developed in the early 1980s. Advances in neuroscientific knowledge have exponentially added to our understanding of the underlying biological basis and neuroanatomy of violence and aggression. Through a binaural sound‐based non‐verbal intervention, we have found a key to unlock long‐term memory (Reconsolidation) that facilitates rapid remediation of anger and violence issues. Within our Pilot Study findings, a number of our combat‐veterans with Post‐Traumatic Stress Disorder (PTSD) experienced a positive transformation in their capacity to evidence empathy, intimacy and social engagement as contrasted with their prior isolative tendencies. We extrapolate how this intervention might positively impact those engaged in Anger Management (AM) and IPV programs. [ABSTRACT FROM AUTHOR]

Objective(s): For a case of severe perfectionism, comorbid with complex trauma symptomatology including suicidality, self‐harming, and other markers of borderline personality, we demonstrate the use of the empirically confirmed process identified in memory reconsolidation (MR) research for the unlearning and nullification, or "erasure," of emotional and behavioral responses driven by learned expectations and mental models. MR has been proposed as a transtheoretical, unifying mechanism underlying profound psychotherapeutic change. The therapist (first author), under the second author's supervision, used a varied set of clinical skills woven together through a focus on the MR process. Results: The result was a depotentiation of underlying, traumatic emotional learnings and near‐total disappearance of perfectionistic and self‐harming behaviors, urges and attitudes after 1 year of therapy. Conclusions: Implications of this case are discussed in terms of symptom generation by implicit emotional learnings and MR as a promising framework for advancing the effectiveness and unification of psychotherapy. [ABSTRACT FROM AUTHOR]

In the mammalian brain, newly acquired memories depend on the hippocampus (HPC) for maintenance and recall, but over time, the neocortex takes over these functions, rendering memories HPC‐independent. The process responsible for this transformation is called systems memory consolidation. Reactivation of a well‐consolidated memory can trigger a temporary return to a HPC‐dependent state, a phenomenon known as systems memory reconsolidation. The neural mechanisms underlying systems memory consolidation and reconsolidation are not well understood. Here, we propose a neural model based on well‐documented mechanisms of synaptic plasticity and stability and describe a computational implementation that demonstrates the model's ability to account for a range of findings from the systems consolidation and reconsolidation literature. We derive several predictions from the computational model and suggest experiments that may test its validity. [ABSTRACT FROM AUTHOR]

Over the past two decades, neurobiology research has added clarity to the process of emotional and behavioral change. In turn, this has led to endorsement of interventions that appear to be most helpful in individual and couple therapy. In addition to research on emotional dysregulation, contemporary studies have focused on the construction of meaning and its relevance to interpersonal relationships. According to Lisa Barrett, Richard Lane, and others, the brain references concepts to rapidly arrive at the most probable conclusions. Encoded experience and memory fragments guide this process and are vital in understanding partners' emotional responses. These findings support an object relations perspective that emphasizes the importance of past relational experiences that inform the present. This is particularly relevant in work with couples, as each individual's beliefs, expectations, and capacity for intimacy are invariably tied to earlier relationships. Research findings on memory reconstruction provide a basis for interventions that can add to the existing treatment approach, as it is suggested that working in a specific way with emotionally based memories has the potential to modify and reduce their predictive power and ability to unleash beliefs and behaviors that work against intimacy. The therapist who is informed by emerging neuroscience research can better uncover and actively work with memories that may be compromising a couple's relationship. [ABSTRACT FROM AUTHOR]

Much of the theoretical focus in post‐traumatic stress disorder has been on the role of the amygdala, the hippocampus and the prefrontal cortex. Crucially, in unresolved traumatic experiences that underlie clinical presentations, this focus misses the brain areas key to the defence responses of fight, flight and freeze—and the associated affects of anger, fear and grief. The periaqueductal gray in the midbrain, with the hypothalamus, is essential for these somatic and emotional responses to traumatic experiences. We argue that when treatment approaches thought to work at the higher brain levels have been ineffective, it is because they have failed to engage the midbrain and hypothalamic sources of the affective responses to the trauma and to the memory of it. Basic affects have been so overwhelming that dissociation, or a similarly protective neurochemical capping mechanism, has prevented full resolution of the affective content of the adversity. Treatment with the Comprehensive Resource Model® (CRM) aims to clear the clinically relevant residues of adverse experiences by resolving the emotional responses accessed through the body memories. When the trauma has led to overwhelming distress, and/or dissociation, there is a necessity for robust resourcing to be in place before the emotional intensity of that distress is accessed. Resourcing needs to be as proximal to the re‐experience as possible to promote complete resolution and in some psychotherapy modalities, the supports provided are somewhat remote from the crucial moments of processing. Therefore, we describe how the CRM seeks to have robustly resourced states present concurrently with traumatised states to avoid overwhelming emotional distress. This allows safe entry into the deepest pain residual from the traumatic event so that it is not overwhelming during processing of the memory, and does not lead to further dissociation, allowing the individual to remain fully present throughout. This "stepping into the affect" can then be so rapidly effective that we also argue that CRM is not an exposure treatment; re‐orientation to the deepest content of the experience resolves the residual distress quickly and permanently through memory reconsolidation. Re‐learning at upper brain levels will then follow from the revoking of the affective power, which has previously driven stimulus/context and response learning in the amygdala, hippocampus and prefrontal cortex. [ABSTRACT FROM AUTHOR]

In addicts, craving and relapse are frequently induced by the recall of memories related to a drug experience. Several studies have demonstrated that drug-related memories are reactivated after exposure to environmental cues and may undergo reconsolidation, a process that can strengthen memories. Thus, reactivation of mnemonic traces provides an opportunity for disrupting memories that contribute to the pathological cycle of addiction. Here we used drug-induced conditioned place preference (CPP) to investigate whether cannabidiol (CBD), a phytocannabinoid, given just after reactivation sessions, would affect reconsolidation of drug-reward memory, reinstatement of morphine-CPP, or conditioned place aversion precipitated by naltrexone in Wistar rats. We found that CBD impaired the reconsolidation of preference for the environment previously paired with both morphine and cocaine. This disruption seems to be persistent, as the preference did not return after further reinstatement induced by priming drug and stress reinstatement. Moreover, in an established morphine-CPP, an injection of CBD after the exposure to a conditioning session led to a significant reduction of both morphine-CPP and subsequent conditioned place aversion precipitated by naltrexone in the same context. Thus, established memories induced by a drug of abuse can be blocked after reactivation of the drug experience. Taken together, these results provide evidence for the disruptive effect of CBD on reconsolidation of contextual drug-related memories and highlight its therapeutic potential to attenuate contextual memories associated with drugs of abuse and consequently to reduce the risk of relapse. [ABSTRACT FROM AUTHOR]

Ample evidence suggests that, when reactivated by a reminder, a consolidated memory may return to a labile state and needs to be stabilized again in order to persist, a process known as reconsolidation. In a previous study, performed in the crab Chasmagnathus, we found a dual role for the biogenic amine octopamine (OA) during memory consolidation. On the one hand, it was necessary for appetitive memory formation and, on the other, it had a deleterious effect on aversive memory consolidation. Thus, OA could be a good candidate to dissect the neurochemical mechanisms of appetitive and aversive reconsolidation. Here, we initially characterized the reconsolidation of an appetitive memory. Then, we compared appetitive reconsolidation with its aversive counterpart regarding the implication of OA in these processes, and contrasted them with previous findings obtained in the consolidation phase. Our results demonstrate that appetitive reconsolidation takes place when animals are re-exposed to the training context, as shown by the amnesic effect of cycloheximide when applied before the reminder. In addition, the no-reinforcement during the reminder is a necessary condition for appetitive reconsolidation to occur. Remarkably, appetitive reconsolidation is neither impaired by OA receptor antagonists nor facilitated by exogenous OA, whereas aversive reconsolidation can be interfered with by OA administration. Thus, our results indicate that appetitive reconsolidation does not involve OA signaling, while aversive reconsolidation is negatively modulated by OA. All in all, these results could constitute a step towards the identification of particular features of appetitive and aversive reconsolidation. [ABSTRACT FROM AUTHOR]

Classical pavlovian conditioning has a major role in the development and persistence of drug addiction. Appetitive conditioning by drug reward, as measured by the conditioned place preference (CPP) paradigm, is an exemplar of classical pavlovian conditioning. Aversive conditioning by footshock involves learning and memory processes similar to those involved in appetitive conditioning. Studies on fear conditioning have shown that long-term fear memory can be extinguished by disruption of reconsolidation of specific memories associated with the fear response. Hence disruption of memory reconsolidation may hold promise for the extinction of maladaptive conditioned behavior. In the present study the effects of the NMDA receptor antagonist, MK-801, and the nNOS inhibitor 7-nitroindazole (7-NI) on memory reconsolidation of cocaine-induced CPP in mice were investigated. We report that, following the acquisition of cocaine CPP, a single acute administration of either MK-801 or 7-NI immediately after retrieval of place preference extinguished subsequent place preference. Moreover, a priming dose of cocaine did not reinstate place preference in the drug-treated groups compared to controls. Male nNOS knockout (KO) mice acquired short-lived cocaine CPP compared to wild-type (WT) mice. A single acute administration of the NO-donor molsidomine to nNOS KO mice immediately after retrieval of CPP prolonged the expression of place preference compared to controls that received saline, suggesting partial strengthening of memory reconsolidation. Taken together, these findings support the role of the NMDAR/NO signaling pathway in memory reconsolidation of cocaine CPP, and suggest that disruption of this pathway during memory reconsolidation may afford resistance to drug-seeking behavior. [ABSTRACT FROM AUTHOR]

Intrusive memories resulting from an emotional trauma are a defining feature of posttraumatic stress disorder (PTSD). Existing studies demonstrate that an increase of noradrenergic activity during a life-threatening event contributes to strengthening or “overconsolidation” of the memory for trauma. The lateral nucleus of the amygdala (LA) is critical for fear learning. Using classical fear conditioning in rats, we have recently demonstrated that noradrenergic blockade in the LA following reactivation of fear memory by retrieval disrupts memory reconsolidation and lastingly impairs fear memory. This suggests that noradrenergic blockade may be useful in attenuating traumatic memories, even well-consolidated old memories, in PTSD. [ABSTRACT FROM AUTHOR]

Memory traces, once established, are no longer sensitive to disruption by metabolic inhibitors. However, memories reactivated by reminder are once again vulnerable, in a time-dependent manner, to amnestic treatment. To determine whether the metabolic events following a reminder recapitulate those following initial training we examined the temporal dynamics of amnesia induced by the protein synthesis inhibitor anisomycin and the glycosylation inhibitor 2-deoxygalactose. The effects of both were transient and dependent on time of reminder post-training and time of injection relative to reminder, and differed from those following initial training. 2-[14C]-deoxyglucose uptake increased in two brain regions, the intermediate medial hyperstriatum ventrale (IMHV) and lobus parolfactorius (LPO) following reminder as it did following training, but the increase was bilateral rather than confined to the left hemisphere and was more marked in LPO than IMHV. C-fos expression after reminder was increased only in the LPO, the chick brain region associated with a late phase of memory processing and recall. Thus although, like initial consolidation, memory processing after reminder is sensitive to inhibitors of protein synthesis and glycosylation, the temporal and pharmacological dynamics indicate differences between these two processes. [ABSTRACT FROM AUTHOR]

Abstract Quantitative in situ hybridization revealed that the expression of the plasticity-associated gene zif268 was increased in specific regions of the rat frontal cortex and nucleus accumbens following fear memory retrieval. Increased expression of zif268 was observed in neurons in the core of the nucleus accumbens during the retrieval of contextual and discrete cued fear associations. In contrast, zif268 expression was additionally induced in neurons of the nucleus accumbens shell and the anterior cingulate cortex during the retrieval of contextual but not cued fear memories. No changes in the expression of this gene were seen in the ventral medial prefrontal cortex or ventral and lateral regions of the orbitofrontal cortex that were correlated specifically with the retrieval of fear memory. These experiments demonstrate the specific and dissociable activation of limbic cortical–ventral striatal regions that accompanies cued and contextual fear. These data, together with those previously published by our laboratory (Hall, J., Thomas, K.L. & Everitt, B.J. (2001) J. Neurosci. , 21 , 2186–2193), suggest that retrieval of contextual fear memories activates a wider limbic cortical–ventral striatal neural circuitry than does retrieval of cued fear memories. Moreover, the expression of zif268 may contribute to plasticity and reconsolidation of fear memory in these dissociable pathways. [ABSTRACT FROM AUTHOR]

In addicts, craving and relapse are frequently induced by the recall of memories related to a drug experience. Several studies have demonstrated that drug-related memories are reactivated after exposure to environmental cues and may undergo reconsolidation, a process that can strengthen memories. Thus, reactivation of mnemonic traces provides an opportunity for disrupting memories that contribute to the pathological cycle of addiction. Here we used drug-induced conditioned place preference (CPP) to investigate whether cannabidiol (CBD), a phytocannabinoid, given just after reactivation sessions, would affect reconsolidation of drug-reward memory, reinstatement of morphine-CPP, or conditioned place aversion precipitated by naltrexone in Wistar rats. We found that CBD impaired the reconsolidation of preference for the environment previously paired with both morphine and cocaine. This disruption seems to be persistent, as the preference did not return after further reinstatement induced by priming drug and stress reinstatement. Moreover, in an established morphine-CPP, an injection of CBD after the exposure to a conditioning session led to a significant reduction of both morphine-CPP and subsequent conditioned place aversion precipitated by naltrexone in the same context. Thus, established memories induced by a drug of abuse can be blocked after reactivation of the drug experience. Taken together, these results provide evidence for the disruptive effect of CBD on reconsolidation of contextual drug-related memories and highlight its therapeutic potential to attenuate contextual memories associated with drugs of abuse and consequently to reduce the risk of relapse., (© 2016 Society for the Study of Addiction.)