Ten Misconceptions of Memory Reconsolidation

Ten Misconceptions of Memory Reconsolidation

Misconception 1.
The reconsolidation process is triggered by the reactivation of a target learning or memory.

Misconception 2.
Disruption of reconsolidation is what erases a target learning.

Misconception 3.
Erasure is brought about during the reconsolidation window by a process of extinction. Reconsolidation is an enhancement of extinction.

Misconception 4.
Anxiety, phobias and PTSD are the symptoms that memory reconsolidation could help to dispel in psychotherapy, but more research must be done before it is clear how reconsolidation can be utilized clinically.

Misconception 5.
Emotional arousal is inherently necessary for inducing the reconsolidation process.

Misconception 6.
What is erased in therapy is the negative emotion that became associated with certain event memories, and this negative emotion is erased by inducing positive emotional responses to replace it.

Misconception 7.
The much older concept of corrective emotional experience already covers everything now being described as reconsolidation and erasure.

Misconception 8.
To induce memory reconsolidation, therapists must follow a set protocol derived from laboratory studies.

Misconception 9.
A long-standing emotional reaction or behavior sometimes ceases permanently in psychotherapy without guiding the steps that bring about erasure through reconsolidation, and this shows that reconsolidation isn’t the only process of transformational change.

Misconception 10.

Carrying out the steps required for reconsolidation and erasure sometimes fails to bring about a transformational change, which means that the reconsolidation process isn’t effective for some emotional learnings.

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Memory Reconsolidation in Context

Memory Reconsolidation in Context

Memory reconsolidation is the brain’s innate process for fundamentally revising an existing learning and the acquired behavioral responses and/or state of mind maintained by that learning. In the reconsolidation process, a target learning is first rendered revisable at the level of its neural encoding, and then revi- sion of its encoding is brought about either through new learning or chemical agents (for reviews see Agren, 2014; Reichelt & Lee, 2013).

Through suitably designed new learning, the target learning’s manifes- tation can be strengthened, weakened, altered in its details, or completely nullified and canceled (erasure) through new learning during the reconsolidation process is the true unlearning of the target learning. When erasure through new learning is carried out in psychotherapy, the client experiences a profound release from the grip of a distressing acquired response (Ecker et al., 2010)

The use of chemical agents to produce erasure is described later in this article. In order to see the full significance of memory reconsolidation for psychotherapy, it is necessary to recognize the extensive role of learning and memory in shaping each person’s unique patterns of behavior, emotion, thoughts, and somatic experience. Among the many types of learning and the many types of memory, the type responsible for the great majority of the problems and symptoms that bring people to psychotherapy is implicit emotional learning—especially the implicit learning of vulnerabilities and sufferings that are urgent to avoid, and how to avoid them. These learnings form usually with no awareness of learning anything, and they form in the presence of strong emotion, which greatly enhances their power and durability (McGaugh, 1989; McGaugh & Roozendaal, 2002; Roozendaal, McEwen, & Chattarji, 2009)

For example, if a small child consistently receives frightening anger from a parent in response to the child expressing needs, the child learns not to express or even feel needs or distress and not to expect understanding or comfort from others. This learning can occur with no representation in conscious thoughts or conceptualization, entirely in the implicit learning system. The child configures him- or herself according to this adaptive learning in order to minimize suffering in that family environment. Later in life, however, this same learned pattern has life-shaping, extremely costly personal consequences.

The learnings in this ex- ample are very well-defined, yet they form and operate with no conscious awareness of the learned pattern or its self-protective, coherent emotional purpose and necessity. From outside of awareness these learnings shape the child’s and later the adult’s behavior, so the individual is completely unaware of living according to these specific learnings.

The neural circuits encoding these learnings are mainly in subcortical regions of implicit memory that store implicit, tacit, emotionally urgent, procedural knowledge, not mainly in neocortical regions of explicit memory that store conscious, episodic, autobiographical, declarative knowledge (Schore, 2003). As in the example above, the vast majority of the unwanted moods, emotions, behaviors, and thoughts that people seek to change in psychotherapy are found to arise from implicit emotional learnings, not in awareness (Toomey & Ecker, 2007).

Common clinical phenomena that express implicit emotional learnings include insecure attachment patterns, family of origin rules and roles, unresolved emotional issues, compulsive behaviors or emotional reactions in response to an external or internal trigger, panic and anxiety attacks, depression, low self-esteem, fear of intimacy, sexual inhibition, traumatic memory and posttraumatic stress symptoms, procrastination, and many others. Of course, some psychological and behavioral symptoms are not caused by emotional learnings— for example, hypothyroidism-induced depression, autism, and biochemical addiction—but it is implicit emotional learnings that therapists and their clients are working to overcome in most cases. There are also genetic or biochemical factors that may contribute to mood disturbances, but it is nevertheless the individual’s implicit emotional learnings that are largely responsible for triggering specific bouts of emotional instability (Toomey & Ecker, 2009).

It is the tenacity of implicit emotional learnings, more than their ubiquity, that is the real clinical chal- lenge. On a daily basis, psychotherapists encounter the extreme durability of original emotional learnings that fully maintain their chokehold decades after they first formed. Researchers too have observed that “A unique feature of preferences [the authors use that term to denote compelling, emotionally complex avoidances and attractions] is that they remain relatively stable over one’s lifetime. This resilience has also been observed experimentally, where . . . acquired preferences appear to be resistant to extinction training protocols” (Pine et al., 2014, p. 1).

The life-constraining grip of such patterns is the bane of psychotherapists and their clients, yet that very tenacity is a survival-positive result of natural selection. In the course of evolution, se-lection pressures crafted the brain so that any learning accompanied by strong emotion becomes encoded by enhanced, exceptionally durable synapses due to the emotion-related hormones that influence synapse formation (McGaugh, 1989; McGaugh & Roozendaal, 2002; Roozendaal et al., 2009). So durable are implicit emotional learnings that they continue to function and drive responses even during states of amnesia and are only temporarily suppressed, not erased, by the process of extinction (nonreinforcement of a reactivated, learned expecta- tion). Psychologists and neuroscientists have amassed extensive evidence that even after complete extinction of an emotionally learned response, the extinguished response is easily retriggered in various ways.

This revealed that extinction training does not result in the unlearning, elimination, or erasure of the suppressed, original learning (making the term “extinction” some- thing of a misnomer, suggesting as it does a permanent disappearance). Rather, the research found that extinction training forms a separate, second learning that competes against, but does not change, the original learning (see, e.g., Bouton, 2004; Foa & McNally, 1996; Milner et al., 1998; Myers & Davis, 2002). The learning formed by extinction training of a fear response is encoded in the brain’s prefrontal cortex, a region that can suppress and temporarily override the nearby subcortical amygdala, which plays a central role in storing and reactivating fear-based learnings (Milad & Quirk, 2002; Phelps, Delgado, Nearing, & LeDoux, 2004; Santini, Ge, Ren, de Ortiz, & Quirk, 2004; Quirk, Likhtik, Pelletier, & Pare, 2003).

Many decades of studying extinction led researchers to the conclusion that implicit emotional learnings are permanent and indelible for the lifetime of the individual once they have been installed in long-term memory circuits through the process of consolidation (reviewed in McGaugh, 2000).

There appeared to exist no form of neuroplasticity capable of unlocking the synapses of consolidated implicit memory circuits. The tenet of indelibility reached its peak influence with the publication of a research article on extinction studies by neuroscientists LeDoux, Romanski, and Xagoraris (1989) titled “Indelibility of Subcortical Emotional Memories.” The indelibility model soon entered the literature of psychotherapy when van der Kolk (1994) published in the Harvard Review of Psychiatry his seminal article “The Body Keeps the Score: Memory and the Evolving Psychobiology of Post- traumatic Stress,” in which there was a section titled “Emotional memories are forever.” The conclusion that implicit emotional learnings persist for a lifetime meant that people could never become fundamentally free of flare-ups of childhood emotional conditioning. The worst experiences in an individual’s past could at any time become reactivated and seize his or her state of mind or behavior in the present. Then, several studies published from 1997 to 2000 suddenly overturned the model of irreversible memory consolidation and indelibility.

Actually, a handful of earlier studies published from 1968 to 1982 had reported observations of the disappearance of well consolidated emotional learnings (Judge & Quartermain, 1982; Lewis, 1979; Lewis, Bregman, & Mahan, 1972; Lewis & Bregman, 1973; Mactutus, Riccio, & Ferek, 1979; Misanin, Miller, & Lewis, 1968; Richardson, Riccio, & Mowrey, 1982; Rubin, 1976; Rubin, Fried, & Franks, 1969). However, these unexplained challenges to the prevailing model of irreversible consolidation were seen as anomalies and received scant attention from memory researchers and clinicians at the time. At the end of the 1990s, however, neuroscientists in several different laboratories resumed studying the effects of reactivating an established emotional learning (Nader, Schafe, & LeDoux, 2000; Przybyslawski, Roullet, & Sara, 1999; Przybyslawski & Sara, 1997; Roullet & Sara, 1998; Sara, 2000; Sekiguchi, Yamada, & Suzuki, 1997).

Using sophisticated new techniques as well as the field’s advanced knowledge of exactly where in the brain certain emotional learnings form and are stored in memory, researchers again demonstrated the full elimination of any expression of a target learning. In addition, they demonstrated that such erasure of the learning became possible because consolidated, locked memory synapses had returned to a deconsolidated, unlocked, unstable or “labile” state, allowing erasure of the learning by chemical agents that disrupt only synapses that are in an unstable, nonconsolidated condition. The longstanding tenet of irreversible consolidation was disconfirmed. The destabilized state of deconsolidation was found to exist only soon after the target learning had been reactivated by a suitable cue or reminder. Yet, long after such a reactivation, an implicit learning is found to be once again in a stable, consolidated state. Thus the detection of a deconsolidated, destabilized state of memory soon after its reactivation implied the existence of a natural process of reconsolidation, the relocking of the synapses of a destabilized memory, returning the memory to stability. Subsequent studies found that the labile state of deconsolidation lasts for about five hours—a period widely known now as the reconsolidation window—during which the unstable target learning can be modified or erased (Duvarci & Nader, 2004; Pedreira, Pérez-Cuesta, & Maldonado, 2002; Pedreira & Maldonado, 2003; Walker, Brake- field, Hobson, & Stickgold, 2003).

If, following the reactivation and destabilization of a target learning, there is no new learning and no chemical treatment, then after its reconsolidation (that is, more than about five hours later) the tar- get learning is found to have increased strength of expression (e.g., Forcato, Fernandeza, & Pedreira, 2014; Inda, Muravieva, & Alberini, 2011; Rossato, Bevilaqua, Medina, Izquierdo, & Cammarota, 2006; Stollhoff, Menzel, & Eisenhardt, 2005).

For that reason, researchers regard reconsolidation as having two biological functions: (a) It preferentially strengthens recent learnings that are most frequently reactivated and destabilized, and (b) it allows new learning experiences to update (strengthen, weaken, modify, or nullify) an existing learning. The latter function is the one utilized for bringing about nullification and transformational change in psychotherapy. When a learned, unwanted emotional reaction is erased, there is no loss of memory of events in one’s life (as shown by Kindt, Soeter, & Vervliet, 2009, and as illustrated by a clinical example later in this article).

There is evidence that the destabilization/restabilization process and the updating/erasure process occur through different molecular and cellular processes (Jarome et al., 2012; Lee et al., 2008). With that background, we can now examine the misconceptions of the reconsolidation process listed above.

The Ten Common Misconceptions of Memory Reconsolidation.

Misconception 1: The Reconsolidation Process Is Triggered by the Reactivation of a Target Learning or Memory As noted earlier, in the reconsolidation discovery studies of 1997 to 2000, a state of deconsolidation was found to exist only soon after the target learning had been reactivated by a suitable cue or reminder. This observation was interpreted by the researchers to

Dispositional Optimism

Dispositional Optimism

'Dispositional optimism, which is defined as the tendency to expect positive vs negative life outcomes (Scheier & Carver, 1992), is a stable, characteristic that has been shown to play a protective role in long-term psychological outcomes.'

 

'In one study of women with early stage breast cancer, optimism was strongly associated with, and predicted changes in, adjustment.  Specifically, individuals exhibiting increased levels of optimism also reported increased levels of subjective well-being, whereas a more pessimistic outlook was associated with poorer adjustment (Carver et all., 1994)'

In another example, Curbow and colleagues examined the role of personal changes and dispositional optimism in the psychological adjustment in long term survivors of bone marrow transplantation (BMT). Results indicated that low levels of optimism were significantly predictive of more negative mood after controlling for both demographic and illness variables.

In another example, in an investigation of the role of optimism in the adjustment of HIV seronegative and seropositive men (i.e., men at risk for developing AIDS), higher levels of optimism were associated with less distress (Taylor et al., 1992)

'Optimism may act as a buffer against stress by influencing the types of coping strategies individuals choose to employ.' (Schier et all., 1986)

Optimists and pessimists use different coping strategies.

Optimists are more adaptive, active, accepting and seek social support.

Pessimists strategies are escape and avoidance.

'In contrast, individuals with a less optimistic outlook are more likely to employ denial and behavioural disengagement as coping techniques which are both associated with increased distress.' (Carver et at., 1993).

 

Effects of Experience Dependent Neural Plasticity

Effects of Experience Dependent Neural Plasticity

The Specificity Effect- Building upon the activity element, interventions need to be specific to the particular cortical function that is the target of behavioural change.  There is a relationship between the nature and type of intervention and the resulting plasticity and modifiability of functions.  This requires assessment, calibration and the provision of varied activities and patterns of intervention.  This has specific implications for the kinds of programs developed must be related both to theory and observations and adjusted accordingly.  The research gives guidance in this regard.  We are encouraged by our review of the research and the identification of critical dimensions of activity to present the Feuerstein Instrumental Enrichment (FIE) program as a paradigm to meet the specificity element (in addition to other dimensions as well), especially when we compared and contrasted to other programs that are available to promote neural plasticity.

The Repetition Effect - Repetition is required for the functional changes to be structurally implanted and manifested in behaviour.  The necessary amount and duration of the repeated exposures is unpredictable, influenced by the nature of functioning, the type of interference, the readiness and skill levels of the participant, the nature of skills being acquired, and the like.  However repetition alone is insufficient.  There must be variation in task structure to promote plasticity-simple redoing of activities without systematic variation is not enough. It appears that repetition cannot be simply re-doing, but must have other characteristics such as novelty, challenge and multi-modality stimulation.

The Intensity Effect - Neural plasticity also requires a degree of intensity of intervention.  These variable relate to the amount of time spent in practice and contact with the intervention modalities.  As with other elements, the specific amount of exposure is hard to predict - some learners need more and others less.  We believe that the production of structural cognitive modifiability requires durations of time and intensity of exposure that typically goes well beyond traditional and accepted patterns of frequency and time duration of sessions.  In our applications (of the FIE program and other MLE related interventions), we expose learners to upwards of 20 hours per week to achieve intended effects.  This contrasts to the typical one or two hours of therapeutic or instructional contact.  In this way the modifiability created becomes established in the neural structures.

The Persistence Effect - Different forms of neural plasticity take place at different times, requiring the provision of both intensity and repetition, which must be reflected in a degree of persistence in treatment planning and implementation over time.  That is, when immediate gains are not evident, one must not give up, but push forward knowing that there is a pace of acquisition that occurs, often latently but eventually materializing.  One is often surprised at the gains that emerge after seemingly endless unproductive encounters.  When they do emerge, they become catalysts for rapid and significant changes.

The Salience Effect - The intervention must be important and meaningful to the individual.  Interventions that do not convey this element will not be responded to as successfully as those that are meaningful.  This has been described as the salience of the intervention.  In the application of the mediated learning experience (MLE) this is the mediation of meaningfulness of that to which the individual is exposed.  Meaningfulness is directly related to creating awareness, which can be considered a sub-goal of the mediation of meaning in that the learner becomes aware of his/her functioning, of its value, of the changes that are experienced, and the importance (value, salience, etc.) of these changes.  Research has shown that this is an important element in neuroplastic activation.  Here too, the importance of assessment and observation must be emphasized to determine what is salient for the learner, and how the learner has internalized what has been learned.  This knowledge guides the mediation regarding intensity, duration, modifiability of stimulation-all of the aspects included in the provision of MLE, and structured into the activities of the FIE programs.

The Optimal Timing Effect - Some kinds of and propensities for change are age related.  For example, although it may be easier to induce plasticity in younger brains, the neurophysiological structures of adult brains and the elderly are also amenable to change, but may require adjustments in aspects of structure and exposure.  The issue is the level of persistence, effort and the types of intervention required to promote plasticity at various ages and stages of development.  In spite of the identification of this element, the research cautions us not to take the dimension of optimal timing as a reason to withhold or not initiate interventions.

The Novelty Effect - Learning experiences must be new and challenging for them to stimulate neural plasticity.  If all one does is repeat familiar tasks, learning will not be facilitated.  Stimulation must challenge the learner and novelty becomes an important aspect of experience.  There is some research showing that simple game activities will not be effective if the interventions do not incorporate the elements of novelty, presenting some degree of challenge and complexity in the tasks.  We have recognized this in the design of the FIE program and the MLE that supports novelty and challenge as learners interact with it.

The Spread of Effect - Changes in functions resulting from a particular intervention can affect changes in other functions not directly targeted by the original intervention.  This has been described as a transference effect, aided by the mirror neuron systems that have been discovered and tracked in neural anatomy.  Specifically, it has been shown in monkeys and humans that activation in one part of the brain will generate activities in other parts, through imitation that excites processes that activate the mirroring mechanisms, often without the individual's awareness or conscious intention.  In the application of MLE, this is described as the parameter of the mediation of transference and must also be embedded in the structure and provision of the intervention.

The Selection Effect - There can be interference, whereby plasticity stimulated or experienced in one area may interfere with changes in other areas.  This must be accounted for in the interventions selected, based on an analysis of the needed behaviour changes and the tasks selected for the intervention.

The Conscious/Awareness Effect - We believe that the learner's awareness of the changes that occur in the process of responding to stimulation is an important aspect of cognitive modifiability.  Exposure should therefore explicitly mediate awareness, and be structured to present opportunities for the learner to reinforce the learning occurring in real time and relate it to other aspects of the learning experience.  This takes the form of "what I have learned, why am I learning it, how will it contribute to further learning, how I have changed, what are my new interests," and many other similar insights.  Even though the individual is not necessarily aware of mirror neuron activity, the changes that occur from such stimulation can certainly be experienced, understood, and related to larger structures of learning.

The Multi-Sensory Effect - Tasks should require perceiving and responding to stimuli from a number of modalities-seeing, hearing, touching and doing.  There is considerable evidence that sensory modalities provide differential and reinforcing stimulation, and are reacted to by different neurophysiological processes, heightening salience, specificity, and selection efforts, which in turn strengthen responding and create new structures.  The brain responds to different sensory experiences, and the mirror neurons activate differential processes in the neural structures, in areas not initially stimulated, but related to the activation.

Activating Modifiability:
Behaviourially and Neurophysiologically

The mechanisms for activation appear to be the direct exposure to stimulation, the imitation of meaningful experience established by the exposure, and a kind of residual effect in the neural system that is the consequence of learning - that is, the structural meaning of prior experience that can be genuinely considered cognitive.  In this sense, these elements- to both understand and activate them-require assessment, and the selection of interventions reflective of both the known elements contributing to neural plasticity and the levels of functioning of the individual to which the interventions are directed.

References:

Principles of Experience-Dependent Neural Plasticity: Implications for Rehabilitation After Brain Damage
The Feuerstein instrumental enrichment program : creating and enhancing cognitive modifiability

Beyond Smarter: Mediated Learning and the Brain's Capacity for Change

Neuroplasticity: Rick Hanson Explains How to Use Our Minds to Change Our Brains

Neuroplasticity: Rick Hanson Explains How to Use Our Minds to Change Our Brains

Author of Hardwiring Happiness, Rick Hanson speaks about how to use your mind to change your brain.
One of the quotes from his book that was particularly impactful to me was ...

'A key aspect of the negativity bias is the special power of fear.  We routinely overestimate threats and underestimate opportunities and resources.  At the same time, negative experiences sensitize the brain to the negative, making it easier to have even more negative experiences in a vicious circle.‘

It can get easier and easier to have negative thought patterns and this vicious circle is something that really has to stop.
And the challenge is to know how to make it stop.  Once that's done, you can decide where you want your own inner programming to go.

 

Belief, Confidence and Hypnosis to Overcome Writers Block and Write Your First Book

 

Marisa Peer: Best-selling Author of 4 books published in 8 languages all over the world. Motivational Speaker and Leading Celebrity Therapist. Voted Best Speaker at Awesomeness Fest Croatia & best therapist in Britain. She works with A-listers, royalty, rock stars & Olympic athletes, all over the world.

She is being interviewed by Chandler Bolt, CEO of the Self-Publishing Summit

Propanolol’s Effects on Long Term Emotional Memory

Propanolol’s Effects on Long Term Emotional Memory

It is well demonstrated that emotion enhances memory encoding and facilitates later recall.1
Such observations have important implications in the realm of psychopathology because many disorders have at their core an overly powerful emotional memory, often stemming from a negative life event.

For instance, in order for posttraumatic stress disorder (PTSD) to develop, one must experience a life threat accompanied by peritraumatic distress.2

During trauma exposure, endogenous stress hormones (i.e., noradrenaline) overconsolidate the traumatic memory.3

This memory is subsequently reactivated too easily by contextual cues, thereby eliciting strong conditioned emotional responses (PTSD, Hormones and Memory) as well as hyper-vigilance and avoidance of trauma reminders.

Numerous psychiatric disorders also have at their core a negative and sometimes traumatic emotional memory. Trauma exposure is known to increase the risk for other disorders, such as phobias, addiction, depression, panic disorder and obsessive–compulsive disorder. (PTSD in treatment resistant obsessive-compulsive disorder.)

Negative life events of lesser magnitude that occur during development or later are also believed to increase the risk for psychopathology. (The role of adversity and stress in psychopathology: some evidence and its implications for theory and research.)

Furthermore, addicted individuals feel unable to resist emotional memories of their past abuse, which manifest in the form of cue-elicited cravings and can contribute to relapse. (Experimental medicine in drug addiction: towards behavioral, cognitive and neurobiological biomarkers).

Thus, decreasing the grip of such powerful emotional memories would seem to have obvious therapeutic value for a whole class of disorders in psychiatry.

One way to decrease the influence of an emotional memory on behaviour would be to interfere with its consolidation, thereby leading to a degraded memory trace.

Memory consolidation refers to the time-dependent process of transferring new learning from short- to long-term memory storage where it is reputed to be permanent.  (Carlson NR. Physiology of behavior. 10th ed. Boston (MA): Allyn & Bacon; 2010. Learning and memory; pp. 440–84)

In a landmark study, Cahill and colleagues (Propanolol effect on long term memory for an emotionally arousing short story)  found that, compared with placebo, propranolol taken before viewing a set of emotionally disturbing slides prevented the heightened recall of those slides.
Since then, many studies have replicated this finding.

The robustness of this finding has been explored in a qualitative review paper, (Nordadrenergic modulation of working memory and emotional memory in humans) but has yet to be investigated by means of meta-analytic review.

In addition to replicating the results of Cahill and colleagues, several researchers have tried to extend them to memory reconsolidation.

Reconsolidation theory (Retrograde amnesia produced by electroconvulsive shock after reactivation of a consolidated memory trace) disputes the permanence of consolidated memories and posits that, in order to persist, a retrieved (i.e., recalled) memory needs to be saved again to long-term memory storage, thereby recapitulating, at least in part, the process of memory consolidation.
(Fear memories require protein synthesis in the amygdala for reconsolidation after retrieval. - LeDoux JE, Schafe GE, Nader K.)

(Attenuation of emotional and nonemotional memories after their reactivation: role of adrenergic receptors. Journal of Neuroscience 1999.)

From a therapeutic point of view, the advantages of blocking reconsolidation rather than consolidation are substantial, since it could allow the otherwise narrow window of opportunity for modifying unwanted memories to be opened at will. (Effect of post-retrieval propranolol on psychophysiologic responding during subsequent script-driven traumatic imagery in post-traumatic stress disorder.)

The substance most frequently used in humans to block memory consolidation and reconsolidation is propranolol.

Propranolol is a synthetic β-adrenergic receptor blocker that crosses the blood–brain barrier and exerts peripheral effects on the noradrenergic system as well as central (inhibitory) effects on protein synthesis.

Propranolol-skeletal.svg

Pro·pran·o·lol prōˈpranlˌôl,-ˌäl/ noun.MEDICINE a synthetic compound that acts as a beta blocker and is used mainly in the treatment of cardiac arrhythmia.

 

(Attenuation of emotional and nonemotional memories after their reactivation: role of beta adrenergic receptors.
Impaired memory consolidation in rats produced with β-adrenergic blockade.
Memory for emotional material: a comparison of central versus peripheral beta blockade. J Psychopharmacol. 1999;13:32–9)

Protein synthesis is necessary to consolidate new learning to long-term memory storage. Animal studies have shown that infusing a protein synthesis inhibitor in the amygdala within the time-limited consolidation window leads to a subsequent memory impairment in a fear conditioning task.
(Protein synthesis and memory: a review. Psychol Bull. 1984;96:518–59.)

Protein synthesis is also required de novo for memory reconsolidation; postretrieval infusions of a protein synthesis inhibitor led to memory impairment of long-term memory, leaving short-term memory intact.
(Fear memories require protein synthesis in the amygdala for reconsolidation after retrieval.)

Propranolol is one of several protein synthesis inhibitors that have been used in animal studies to reduce the saliency of emotional memories.
(Fear memories require protein synthesis in the amygdala for reconsolidation after retrieval. Nature. 2000;406:722–6.)

Attenuation of emotional and nonemotional memories after their reactivation: role of beta adrenergic receptors.

(Impaired memory consolidation in rats produced with β-adrenergic blockade.)

(Disruption of reconsolidation but not consolidation of auditory fear conditioning by noradrenergic blockade in the amygdala.)

A neuroimaging study revealed altered amygdala and hippocampus activity associated with propranolol-induced emotional memory impairment in healthy individuals.  (Neural signature of reconsolidation impairments by propranolol in humans)

Propranolol is commonly used to treat migraine, tachycardia and performance anxiety.
(Propranolol in the management of recurrent migraine: a meta-analytic review.)
(Propranolol decreases tachycardia and improves symptoms in the postural tachycardia syndrome: Less is more)
(Effect of beta blockade and beta stimulation on stage fright.Am J Med)

It is also indicated as a second-line therapy for anxious states because of its effects on the noradrenergic system.

It reduces the flow of norepinephrine in certain parts of the brain.
Norepinephrine focuses your attention.
Going a bit further into the chemical train and there occurs a process of protein synthesis leading to the structure of long term memory.
So when you affect the flow of norepinephrine, ultimately you are affecting wether or not memories are consolidated which leads to the structure of long term memory.

Effecting the structure of long term memory through interventions that initiate memory reconsolidation can be epically transformative for clients that are seeking improvements in behaviours and overall life performance.

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