Fear Memory Essay

The hippocampus, memory and organization portion of the brain, and the amygdala, the “fight or flight” portion, are both confused by PTSD (“PTSD and The Brain”, 2-3). For example, if an Iraqi soldier hears a helicopter overhead, the hippocampus remembers the sound of the helicopter and works with the amygdala to associate that noise with a traumatic war event. The amygdala then will induct a fight or flight response, causing symptoms of PTSD to initiate. (Ibid, 3) While symptoms can be difficult, the hardest part of having PTSD, is sometimes admitting you have a disorder.

The amygdala, though, is involved not just in the fear response, but in the memory of fear, as well. In one test, researchers used functional MRI scans to measure amygdala activity while showing subjects a number of frightening and neutral images. They found that the degree of amygdala activity was a good predictor of both fear level (as reported by the subject) and of the ability several weeks later to recall having seen the image (1).

The article, Concussive brain injury enhances fear learning and excitatory processes in the amygdala by Maxine L. Reger, Andrew M. Poulos, Floyd Buen, Christopher C. Giza, David A. Hovda, and Michael S Fanselow took a close look into the fears and behaviors generated in rats two days after suffering trauma to the brain. This particular article was discovered by searching the keywords: brain injury and amygdala, in the PubMed database. By searching those keywords, the database was able to pull up numerous articles discussing the two topics, but I felt that Reger et al (2012) demonstrated a clear association between the topics. The article brings about a question of whether or not there is a link between brain injuries, posttraumatic stress disorder, commonly referred to as PTSD, and the changes involved in the excitatory and inhibitory processes involved in the amygdala. In order to examine such a link, the authors performed a number of tests on adult Sprague-Dawley rats to test their hypothesis as well as to investigate the neurobiological correlation between concussion and PTSD. To further assess these correlations, it is imperative to explore the methods used to conduct this study.

Studying the brain has been an affective result in finding out the various neurochemicals that are involved with PTSD. Brain imaging systems nowadays focus on two brain structures, the amygdala and the hippocampus. The amygdala is involved with how we learn about our fear and hippocampus plays a role with our memory formation. Some research focuses on a hormonal system known as hypothalamic-pituitary

Post-traumatic stress disorder was officially classified approximately three decades ago. Considering its relatively recent discovery, the complete etiology and optimal biological therapies are yet to be elucidated. This review examines the neural correlates and biomarkers of PTSD along with biological therapy options. Studies revealed that hypoactivation of the ACC and hyperactivation of the amygdala are consistent with PTSD, suggesting that the prefrontal cortex may be increasingly unable to regulate the emotional processes of the amygdala.

Because this process in the brain is so sensitive, lots of things can alter it and mess with the “creation and storage” as well everything that makes the thinking part of the brain conscious (Howard & Crandall, page 10). If something does interfere or disrupt with the regulatory processes of the brain, such as danger, or any traumatic experience in this case, the amygdala determines that danger is present. Trauma will trigger the “flight or fight” sequence as well as set off stress hormones that raise adrenaline, including blood pressure and heart rate. While one interference, depending on the amount of fear a person has, may not hurt the brain at once, “if the trauma is prolonged, extreme or repetitive, it can physically injure the brain” (Howard & Crandall, page 14). In the process of damaging the brain, there will be damages done to the automatic system as well, including disturbances in sleep, such as dreams or nightmares.

On the brain of a mammal, once external stimuli affects a person, pressure is put on the paraventricular nucleus of the thalamus. The paraventricular thalamus (PVT) is a stress sensor that is activated once influenced by physical and psychological stressors. Studies show that the paraventricular nucleus of the thalamus controls a part of the amygdala, and the interaction between the neurons of the central amygdala and the paraventricular nucleus of the thalamus is a step towards modulation of fear as it forms a stable foundation of fear memory and manifestation of response to fear.

Stout’s description of how the brain reacts under stress shows how traumatic memories can become lost or disorganized. Trauma has a significant impact on stress-responsive neurohormones, which are hormones produced by the nervous system. Trauma causes the areas of the brain involved in

In normal brain functioning and NE levels, alpha-2 receptors are strongly stimulated and PFC performance is enhanced, whilst amygdala function is reduced. By blocking alpha-1 receptors or stimulating alpha-2 receptors, stress symptoms can be relieved. Because of this, alpha-1 receptor antagonists and alpha-2 receptor stimulants have been explored for the treatment of PTSD. A successful alpha-1 receptor antagonist that has been used in various studies of PTSD treatment in adults is prazosin. Several studies have shown that prazosin significantly reduces symptoms of PTSD in adults, nightmares and sleep disturbance in particular, and improved the overall wellbeing of patients (5-10).

Many scientists have been turning to genes that may have a role in creating fearful memories for an explanation as to what causes PTSD. They have also been studying different areas of the brain that control fear and stress such as the amygdala and prefrontal cortex. The amygdala has a role in the early stages of learning to fear and not to fear certain situations. The prefrontal cortex is said to help control the extinction of long term fearful memories. An individual genetics, brain area growth, and other environmental factors play a role in the risk of the individual developing PTSD after a traumatic

These findings have come from an experiment that compared BI rats (Wistar Kyoto) and non-BI rats (Sprague-Dawley). WKY rats demonstrate enhanced active avoidance acquisition which contributed to their inability to extinguish avoidant responses to warning signals even after the aversive stimulus has been eliminated (Servatius, Jiao, Beck, Pang, & Minor, 2008). WKY rat’s resistance to extinction of avoidant behaviors is a principal component of WKY’s ability to overcome the ‘warm up’ effect. Thus, WKY rats warm-up decrement exhibits pervasiveness of learned avoidance behaviors and is a key component of their abnormal avoidant behavior (Servatius, Jiao, Beck, Pang, & Minor, 2008). The avoidance acquisition that has been demonstrated with WKY rats is a type of learning similar to the learning involved in PTSD. PTSD has been hypothesized to occur through enhanced associative learning of an avoidant response to an earlier traumatic event (Allen & Miller, 2016). Thus, BI and avoidance are closely related to the formation of PTSD. WKY rats showed little evidence of warm-up, resulting in them being selectively insensitive to changes in the response contingency. We hypothesized that enhanced acquisition of avoidance responses in WKY rats is a result of their enhanced amygdala activation, therefore we predict that amygdala lesions will decrease the rate of

The amygdala is known to learn from exposure to fear and store assessment of threat–related stimuli. The prefrontal cortex is involved in extinction and the retention of fear and is connected to the amygdala. Finally, the hippocampus encodes the context during fear learning process and sends it to the amygdala. People with PTSD have hyper-activity in the amygdala, while having hypo-activity in the prefrontal cortex and there is reduction of the hippocampus volume. This reduction may limit proper evaluation and categorization of the experience. A study on Vietnam soldiers revealed that lesions in the amygdala and prefrontal cortex resulted in the absence of PTSD. To get further into the molecular level studies been done on the hormonal system. “Stress is known to contribute to the pathogenesis of a variety of disorders, including the majority of psychiatric like major depression and posttraumatic stress disorder.” (http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3825244/pdf/DM30-02-343616.pdf). Research has revealed evidence that a hormonal system known as the hypothalamic-pituitary-adrenal (HPA) axis is the one that gets disrupted in people with PTSD. The hormonal system is involved in normal stress reactions, so the disruption of this system in people with PTSD creates this “false alarm”. It has been suggested by some scientist that the dysfunction of the HPA system results in hippocampal damage in people with PTSD. Damage in the hormones is caused by damage to

To continue the research, Jordan Smoller distinguishes this section of the genetics of anxiety, “…the majority of the genetic association studies of the anxiety disorders have been candidate gene studies based on a limited number of biological hypotheses. [These are] commonly focused on genes related to monoaminergic neurotransmitter systems [(refer to the particular neurotransmitters dopamine, noradrenaline, and serotonin)], neuropeptides, and HPA axis function [(hypothalaic-pituitary-adrenal axis)]” (Smoller, p. 308). Individually, settled test creature models catch critical parts of human nervousness and dread conduct, and neuroimaging considers have gained free ground in mapping the primary and practical segments of uneasiness/fear symptoms.

Here, predictive learning and associative fear memory come together to create the fear driven anxiety, based upon fear of the subject’s predicted consequence. Based on previous research, it is thought that disrupting this reconsolidation of fear memories can lead to an effective treatment for PTSD and anxiety disorders. In past research it has been found that by using the noradrenergic Beta-blocker propranolol HCl one can disrupt the reconsolidation of fear memory without affecting expectancy learning. Propranolol HCl is used because it is able to pass through the blood brain barrier and block Beta-adrenergic receptors present on the amygdala (affecting the neuroplasticity of memory formation). It is still a question as to if this type of experimental model will work for fear conditioning. The emotional process is very complicated and researchers wonder if the addition of fear and anxiety into the memory will complicate the process of disrupting reconsolidation. In animal models of this experiment, it appears that the older and stronger memories are harder to reconsolidate than newer and weaker

The capacity to form memory in face of stressful stimuli is an essential adaptive behaviour that enables organisms to respond rapidly and effectively to similar demands1. The stress response is largely mediated by the hypothalamic-pituitary-adrenocortical axis (HPA) coupled with the release of catecholamines through adrenergic neural discharges1. These physiological mechanisms activate downstream pathways that stimulate metabotropic alterations in neural networks, resulting in long-term memory formation1. In animals and humans, stress mediated neuroendocrine responses enhance the consolidation of emotional memories2. However, exposure to traumatic or chronic stress can result in memory impairments as well as memory related psychopathologies such as posttraumatic stress disorder (PTSD) 1. Noradrenergic mechanisms are largely implicated in the mediation of emotional memory consolidation1. Therefore, the disruption of this mechanism during periods when memories are in a molecularly labile state has been proposed as a clinical method of pharmacologic modification of intolerable memories in psychiatric patients3. The application of β-adrenergic receptor antagonists during periods of memory reconsolidation is a possible novel mechanism of emotional memory modification in patients with memory related psychopathologies4. In this paper, the influence of the noradrenergic receptor antagonists, propranolol, on stress mediated memory reconsolidation will be characterized. Similarly,