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Introduction and Background Information

Question:

Discuss about the Mechanisms of Fear Memory Extinction and Psychological Therapeutic Approaches.

Fear is an emotion that exists in both human and animals, and it is easier to understand by studying brain mechanisms.  In psychiatric conditions, the condition plays a critical role, and because of this, it is critical to understand its neural basis.   Fear occurs when one is subjected to conditions that result into intimidating environmental states. Current research puts great emphasis on Pavlovian fear condition. This analysis involves measuring conditioned responses that an auditory conditioned stimulus exhibits when the memory test is underway, which is almost the same as real life experiences where an unconditioned stimulus (US) causes some harm and then the conditioned stimulus (CS) takes place about the painful stimulus.  This is always the case when a cat wounds a rat but it escapes. The rat forms a memory of some noise or rustling of grass that occurred when the cat was about to pounce on it.

This paper examines recent studies on both molecular and cellular mechanism that often result into auditory fear conditioning.  While molecular changes do  take place in many areas of the amygdala, the paper will focus on lateral (LA) nucleus as there is adequate prove that molecular change in this place contributes significantly to the acquisition, consolidation, and memory expression.  Given that unique molecular mechanisms underscore stages of memory formation, this analysis will is based on Pavlov’s dog and rodent research and is organized according to the three stages, acquisition, consolidation, and then reconsolidation of memories. Additionally, it presents the limitation of extinction.

Pavlov started the processes of discovering the Pavlovian conditioning theory when he saw a dog salivate. He first thought that dogs do not need to learn to do some things such as salivating when they see food. In behavioral terms, this means food is unconditional stimulus while salivating in unconditional response. Pavlov proved this is presenting his dog with a bowl of food and measuring its salivary secretions. Later, he also learned that the dog would produce the same amount of salivary secretions when it saw the lab assistant; he concluded that he had discovered a conditioned response. Pavlov chose to ring a bell whenever he presented the food. He recorded the same response (Pavlov, 1902).

Memory exists when people learn. When observing molecules that initiate memory function, it appears true that there can be no memory whenever there is not learning as there is nothing to store in the brain. An understanding of LA mechanism of fear memory formation can help to appreciate how memory acquisition occurs. Consequently, it will analyze the application of rodent studies in humans followed by extinction-based strategies (Pavlov, 1902).

The Hebbian mechanism, which is based on the findings of Hebb, is a common mechanism at this juncture. A common view based on it emerged in neuroscience that explains how a synaptic input can be enhanced (Learning Rule, 2008).  This LA mechanism provides that when activities take place in the presynaptic neuron, a simultaneously activity occurs in the postsynaptic neuron, it becomes possible to strengthen a synaptic input.  This relationship with the strong inputs strengthens the weak one (Kwok, 2009). One thing that Hebbian Plasticity does not guarantee, according to new evidence, is that LA can explain fear conditioning entirely (Pape and Pare, 2010).

Molecular and Cellular Mechanisms of Auditory Fear Conditioning

While Hebb explicitly explains how plasticity can occur during the acquisition stage, it fails to comprehensively explain learning, particularly learning that type of learning that occurs in highly charged emotional environments.  This has led to the emergence of neuromodulatory-dependent mechanisms (Schiller et al., 2013).

Recent research suggests that monoamine transmitters are responsible for regulating glutamatergic transmission as well as Hebbian plasticity (Tully and Bolshakov, 2010).

Another credible evidence points to the fact that neuromodulatory regulation of this mechanism can lead to the development of plasticity and fear learning. Neurons in the LC, as well as substantial nigra, are activated by the USS and CSs.  Consequently, after the presentation of aversive stimuli, the amount of NE and DA increases in the amygdala (Guzman-Karlsson et al., 2014). The conclusion here is that NE and DA have the ability to modulate the acquisition of fear learning.

This term “consolidation” refers to the process of stabilization of temporary STMs into persistent STMs.  Covalent modification of synaptic proteins is responsible for mediating plasticity that is essential for both STM and immediate learning.  However, research has shown that the consolidation of this plasticity occurs through activation of second messengers.  Alberini et al. (2009) provide that these messengers initiate the process of gene transcription and also a translation of new proteins. This research finding makes it clear that both neuromodulatory and Hebbian mechanisms play the role of implementing the original intracellular activities. However, they can as well prompt the sending of the messengers. As already indicated above, molecules that make STM possible are the ones involved in memory consolidation (Sacktor, 2008).

Recent studies show that kinase is involved in memory maintenance.  Sacktor’s works show that an atypical isoform of PKC is responsible for this task. Inhibition of this isoform in the LA after a fear learning experience clears fear memories (Sacktor, 2008). According to Jensen et al. (2009), it is true that the isoform of PKC maintains, and it may be doing this by reducing GluA2 AMPAR subunit removal, which ultimately results to the sustainability of the synaptic strengthening that the fear learning originally induced.

After learning, fear memories are consolidated and store.  However, they can be labile when reconsolidated.  During the process of reconsolidation, the presentation of memory that is related with the environmental cue, for example, conditioned CS to activate memories and that also makes them labile. If a behavioral manipulation following memory reactivation occurs following memory activation such as post-training manipulations, the new labile memory is transformed (Shih  & Wu, 2017; Agren et al., 2017).

In many past instances, the study of reconsolidation has been undertaken through systematic pharmacological manipulations. A finding by Sara reveals that the disruption of the consolidation of STM is done by protein synthesis stoppage in the LA (Elsey  & Kindt, 2017). Schafe and his counterparts also led the research that discovered that blockade of protein synthesis also affected reconsideration adversely subsequent to the recovery of well-consolidated fear memories (Schafe et al., 2001).

These series of research have caught the attention of many people.  Researchers need to consider using auditory fear conditioning to examine these processes as the understanding about fear memory consolidation is at an advanced stage. However, going by the available research, it is apparent that blockade of reconsolidation helps to bring down auditory conditioned and unconditioned stimulus that is evoked by neural responses. This means that when reconsolidation is blocked, auditory thalamic inputs to LA neurons are potentiated (Alberini et al., 2013; Agren et al., 2017).  The modification of the memory using reconsolidation-related extinction has provided several positive outcomes. 

Mechanisms of Memory Formation

Recent research has demonstrated how prefrontal cortex and hippocampus interact and affect memory retrieval and consolidation. In a successive Go/No-Go training of rats, Gilbert and Kesner (2004) investigated the role of the hippocampus and (medial prefrontal cortex) mPFC in spatial paired-associate learning. They discovered that rats with ibotenic acid-based lesions in the hippocampus had signs of irrecoverable performance impairment in location-in-place and object-in-place arms. However, when these researchers inactivated mPFC using muscimol in normal animals with intact hippocampi, the same severe impairment seen in “object-in-place” arms was registered. This experiment confirmed that the hippocampus is needed for a biconditional paired-associate task when space is required. On the other hand, the mPFC is more selectively involved in the object-pace paired-associate task than in any other tasks (Schiller at al., 2013).

A lot of evidence suggests that fear memory reconsolidation can be blocked; the testing has been done on animals only. However, two recent studies have given encouraging results for reconsolidation of emotional memories in some patients as well as in healthy volunteers (Keum & Shin, 2016). The slow pace of human reconsolidation research has been brought about by the fact that many compounds that are used to block reconsolidation in animals are toxic to humans. Besides, pharmacological agents could adversely affect different measures of fear in man (Schiller at al., 2013).

The encouraging results in results led Schiller and his team to try to translate combined reconsolidation and extinction techniques to humans (Schiller at al., 2013). They successfully replicated the finding that extinction training carried out ten minutes after reactivation (the reconsideration window) reduced fear, but it did not lead to spontaneous recovery or returned following a reinstated shock.  The reduction in fear achieved from the reconsolidation- extinction techniques took only one year and relapsed. From a clinical standpoint, the results are encouraging. However, as at now, it is impossible to tell whether the techniques can change traumatic memories in patients suffering from various traumatic disorders such as anxiety disorders (Agren et al., 2017).

The boundary that has existed between the basic and clinical research has begun to become smaller given the development in extinction and reconsolidation research.  The increasing use of DCS to facilitate extinction was developed from rodent studies. Today, they are showing promise in studies for social anxiety disorder, phobia, OCD, and PTSD. Since it strengthens extinction, pharmacologically adjusts can reduce the relapse of fear memory. As the rodent studies suggest,   many other compounds are can be used to strengthen or accelerate extinction. Some of them, according to researchers Graham and Richardson (2010) are fibroblast growth factor, yohimbine, and methylene blue. Other recent studies may provide the solution.  One of them has suggested that extinction can be adduced by purely pharmacological means (Lissek et al., 2013).

The rodent studies revealed that extinction in young rodents led to paradoxical approach behaviors to the CS.  When researchers conditioned rats to fear simple tones by associating them with electronic shock, they began the extinction phase. They discovered that more BLA-NAC activity could lead to extinction learning. When they gave rats food in the presences of the previously feared tone, this resulted in decreased spontaneous recovery of fear.  The amygdala modulates the fear response in many functional magnetic resonance imagings (fMRI). This discovery can be used to treat childhood traumas.  Research shows these strategies have been effective in children. The rodent study show that the development switches that control the permanence of these memories can be changed successfully (Lissek et al., 2013).

Hebbian Mechanism and Neuromodulatory-Dependent Mechanisms

The amygdale is well-known for playing a central role in the acquisition and expression of fear. Recent research has, however, implicated it in the extinction of fear memories. According to research, the amygdala corporate is regulated by the venromedial prefrontal cortex (PFCvm). When the hippocampus learns about the context of acquisition, it modulates the expression and extinction of the memories in relation to that particular context (Fuster, 2015).

Clinical treatment based on extinction has proven that this approach has several weaknesses.  First, it relies on negative prediction errors that only be depended on if the CS predicted the US consistently.  In most cases, highly feared outcomes take place infrequently or do not take place at all. A man who fears the heights, for example, can maintain fear despite never falling (Agren et al., 2017).

The next limitation is that there is always a little correlation between memory strength and behavioral measures. A fear condition in rodents, for instance, clearly shows that between-session recovery of the CT cannot be predicted by within-session decreases in the CR. Extinction procedures also render the CS ambiguous. This may lead to unfavorable a situation for people with a verse ambiguity and uncertainty. Research has found that people with high self-reported intolerance of uncertainty express higher spontaneous recovery after extinction (Agren et al., 2017).

Extinction can also relapse and is highly dependent on the context in which it occurs.  By combining extinction and reconsolidation, it is possible to have a greater understanding of this concept. Intracellular processes can evidently interfere with reconsolidation after memory retrieval.  However, there is also evidence that behavioral manipulations after memory reactivation can also change the memory of fear. A good example is extinction training.  Through repeated presentation of the stimulus without using the US, this training helps to bring temporal memory extinction.  If the same individual is exposed to a new context or the US, the memory can be revived. Extinction, therefore, often do not generalize beyond the therapy room, which is the cause of high relapse rates for PTSD and anxiety (Agren et al., 2017).

Conclusion

The last few decades have witnessed a significant increase in the interest of medical experts in the neural mechanisms of Pavlovian extinction.  With adequate extinction, rats, people, and other subjects respond to the conditioned stimulus in a manner that suggests they have never been conditioned. As this analysis has demonstrated, many recent research studies have indicated that extinguished fear responses relapse following an aversive event, with time, or when the conditioned stimulus is presented in a different context, which is behavioral evidence that extinguishing fear does not erase all the memories.  All it does is generate an inhibitory memory that temporarily suppresses the expression of fear. This paper has revealed that many modern researchers characterize the neural mechanism of inhibition, focus on the amygdala, hippocampus as well as prefrontal cortex to try to solve the problem of memory fears.  Since this theory allows for a relapse, it is clearly not effective.  The remedy, for that reason, is for experts to continue working on finding advanced behavioral methods that can modify the original fear memory permanently.

References

Agren, T., Björkstrand, J., & Fredrikson, M. (2017). Disruption of human fear reconsolidation using imaginal and in vivo extinction. Behavioural Brain Research, 319, 9-15. doi:10.1016/j.bbr.2016.11.014

Alberini, C. M., Johnson, S. A., & Ye, X. (2013). Memory Reconsolidation. Memory Reconsolidation, 81-117. doi:10.1016/b978-0-12-386892-3.00005-6

Elsey, J. W., & Kindt, M. (2017). Tackling maladaptive memories through reconsolidation: From neural to clinical science. Neurobiology of Learning and Memory. doi:10.1016/j.nlm.2017.03.007

Fuster, J. M. (2015). Anatomy of the Prefrontal Cortex. The Prefrontal Cortex, 9-62. doi:10.1016/b978-0-12-407815-4.00002-7

Gilbert, P. E., & Kesner, R. P. (2004, January). Memory for objects and their locations: the role of the hippocampus in retention of object-place associations. Retrieved May 13, 2017, from https://www.ncbi.nlm.nih.gov/pubmed/14670357

Graham, B. M., & Richardson, R. (2010). Fibroblast Growth Factor-2 Enhances Extinction and Reduces Renewal of Conditioned Fear. Neuropsychopharmacology, 35(6), 1348-1355. doi:10.1038/npp.2010.3

Guzman-Karlsson, M. C., Meadows, J. P., Gavin, C. F., Hablitz, J. J., & Sweatt, J. D. (2014). Transcriptional and epigenetic regulation of Hebbian and non-Hebbian plasticity. Neuropharmacology, 80, 3-17. doi:10.1016/j.neuropharm.2014.01.001

Jensen, T. E., Maarbjerg, S. J., Rose, A. J., Leitges, M., & Richter, E. A. (2009). Knockout of the predominant conventional PKC isoform, PKC , in mouse skeletal muscle does not affect contraction-stimulated glucose uptake. AJP: Endocrinology and Metabolism, 297(2). doi:10.1152/ajpendo.90610.2008

Keum, S., & Shin, H. (2016). Rodent models for studying empathy. Neurobiology of Learning and Memory, 135, 22-26. doi:10.1016/j.nlm.2016.07.022

Kwok, S. M. (2009). In vivo visualization of CaMKII activity in ocular dominance plasticity.

Lissek, S., Glaubitz, B., Uengoer, M., & Tegenthoff, M. (2013). Hippocampal activation during extinction learning predicts occurrence of the renewal effect in extinction recall. NeuroImage, 81, 131-143. doi:10.1016/j.neuroimage.2013.05.025

Nagarkatti, N., Deshpande, L., & Delorenzo, R. (2009). PLASTICITY | The Role of Calcium in Mediating Neuronal Plasticity in Epileptogenesis. Encyclopedia of Basic Epilepsy Research, 1181-1189. doi:10.1016/b978-012373961-2.00324-6

Pape, H., & Pare, D. (2010, April). Plastic Synaptic Networks of the Amygdala for the Acquisition, Expression, and Extinction of Conditioned Fear. Retrieved May 11, 2017, from https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2856122/

Pavlov, I. P. (1902). The work of the digestive glands. London: Griffin.

Sacktor, T. C. (n.d.). PKMzeta, LTP maintenance, and the dynamic molecular biology of memory storage. Retrieved May 11, 2017, from https://www.ncbi.nlm.nih.gov/pubmed/18394466

Schafe, G. E., Nader, K., Blair, H. T., & LeDoux, J. E. (2001, September). Memory consolidation of Pavlovian fear conditioning: a cellular and molecular perspective. Retrieved May 11, 2017, from https://www.ncbi.nlm.nih.gov/pubmed/11506888

Schiller, D., Kanen, J. W., Ledoux, J. E., Monfils, M., & Phelps, E. A. (2013). Extinction during reconsolidation of threat memory diminishes prefrontal cortex involvement. Proceedings of the National Academy of Sciences, 110(50), 20040-20045. doi:10.1073/pnas.1320322110

Shih, M., & Wu, C. (2017). Gap Junctions Underlying Labile Memory. Network Functions and Plasticity, 31-50. doi:10.1016/b978-0-12-803471-2.00003-5

Tsukada, M. (2008). Interaction Between the Spatio-Temporal Learning Rule (Non Hebbian) and Hebbian in Single Cells: A Cellular Mechanism of Reinforcement Learning. INTECH Open Access Publisher.

Tully, K., & Bolshakov, V. Y. (2010, May 13). Emotional enhancement of memory: how norepinephrine enables synaptic plasticity. Retrieved May 11, 2017, from https://www.ncbi.nlm.nih.gov/pubmed/20465834

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