Amygdala Experiment

While on patrol, I was parked in the entrance to Mansard's plaza, facing E Ridge Rd, monitoring traffic. A female in a silver pickup truck pulled into the lot and flagged me down. The female pointed towards a white and maroon Corvette traveling east on Ridge Rd and stated that she believes the driver may be intoxicated. I immediately pulled onto Ridge Rd and got behind the Corvette. As I was following the Corvette east on Ridge, another vehicle with a male driver pulled up to the side of me and shouted out the window, "That guy is drunk". I then observed the Corvette to weave from the outside lane to the center lane, without signaling. The vehicle then abruptly swerved back into the outside lane, without signaling. The vehicle then came to

The amygdala specializes in threat detection, fear, excitement, and arousal, hippocampus helps format long-term declarative memories and spatial reasoning. The anterior cingulate cortex influences autonomic function, decision making, error detection and emotion while the posterior has a role in spatial annotations memory. The septal area produces pleasurable feeling,

Signal processing within the amygdala is further regulated by interactions with a network of external structures. In particular, the dMT and its projections to the CeL have been demonstrated to play a role in fear memory retrieval. Notably, the dMT is assumed to be extensively modulated by opioids considering its innervation with opioidergic fibers and the high expression levels of MORs. Previous studies have reported the MOR system in the PVT, as part of the dMT, to be involved in managing physical pain. Moreover, social pain, which describes social rejection, being excluded or not being liked by others and which is associated with symptoms of anxiety and depression, appears to involve the MOR system in the PVT (Hsu et al). However, so far a direct implication of

The purpose of this experiment is to examine the functional role the dorsal periaqueductal gray (PAG) plays in initiating fear behavior by associative auditory and context fear conditioning. The dorsal PAG has been previously studied to coordinate defensive behavior via a freezing response. It has been noted that the dPAG relays unconditioned stimulus information to the basolateral amygdalar complex (BLA), which directs learned and innate responses to fear and that the neuronal activity spike rates evoked are modulated by context (Kim et al, 2013). After linking the dPAG’s relationship in fear conditioning, it is hypothesized that if the dPAG is necessary for associative fear conditioning, then after several paired unconditioned and conditioned stimuli trials, neuronal firing should augment in the dPAG. Moreover, in an additional experiment, after considering NMDA’s high associability with glutamate (excitatory neurotransmitter), it is predicted that the infusion of NMDA-R inhibitor within the dPAG will block excitation of the structure and function, which may lead to little to no freezing behavior when presented with the conditioned stimuli.

All the experiments performed by Rau, Decola, & Fanselow support a phenomenon in which prior exposure to several shocks enhances subsequence learning of conditional fear. Based on the data they suggested that this effect occurs because the potent pre-shock experience sensitized the subject’s susceptibility to acquire conditional fear. It also proves that this procedure may serve as a model of specific components of PTSD. This series of experiment provides insight into the possible treatments for PTSD. Neither behavioral nor pharmacological elimination of the fear to the original traumatic context was capable of alleviating the effects of the stressor. It will is important for future studies to determine the mechanisms for this sensitization, which will be able to provide a complete treatment for PTSD.

Two structures in the brain work independently and with each other to impact memory and emotions: the amygdala and the hippocampus. The amygdala is linked to fear-conditioning, while the hippocampus is linked to episodic memories, which are those memories that a person can recall whenever wanted [1]. An experiment was performed to demonstrate the independence of the two structures from each other which involved patients with lesions in the amygdala and patients with lesions in the hippocampus. Researchers designed a fear-condition wherein a blue patch applied to the wrist initiated a shock. They found that patients with lesions in the amygdala had no physiological response to the conditioned stimulus (the blue patch) [2], whereas patients with lesions in the hippocampus demonstrated appropriate

According to the article by Schaffhausen, the brain has two basic requirements to learn a fear. The first one is the sensory systems, such as the visual system for a light or the tactile system for a shock. The second area is the amygdala as a critical region for fear conditioning. “The amygdala is a small, almond-shaped cluster of nuclei set deep in the temporal lobe that seems ideally positioned as the locus of fear learning. It receives input through its lateral nucleus from cortical areas and the thalamus, which is a key sensory relay station within the brain, and it sends output via its central nucleus to a variety of brain regions that are known to mediate fear responses, such as the hypothalamus.” (Schaffhausen.2005). The crucial role for the amygdala in fear conditioning that if it is destroyed, it will still show a fear response but fail to learn the association between the sensory systems, such as the light and the brain regions that are known to control fear responses. Consequently, the amygdala is a key structure for fear

DQ: People with amygdala damage approach other people indiscriminately, instead of trying to choose people who look friendly and trustworthy. What might be a possible explanation?

Current study focuses on the understanding of Molecular Mechanism of Pavlovian conditioning (PC). Pavlovian conditioning is the reference paradigm for the study of associative learning based on the programmed relation of two stimuli, the conditioned stimulus (CS), a tone, and the unconditioned stimulus (US), sucrose-water. Previous research in rodents has revealed that the limbic circuits (or BLA), play an important role in Pavlovian reward learning. We hypothesize that PC acquisition produces a different memory from PC extinction in the BLA. In this study some of the markers analyzed and measured include: atypical Protein Kinase M ζ (PKMζ), Protein Kinase C ι/λ (PKC ι/λ), AMPA (a-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid) receptor subunits glutamate A1 (GluA1), GluA2 and GluA3.These markers are important for consolidation and retrieval of memory.

Neuroscientists believe that free will is an illusion; that our actions are determined by brain movement beyond our control. Neuroscientist such as Libet and Hayne believe that the activity in the brain comes before we consciously act. They did several experiments, which included people pressing buttons with either their left or right hand. The aim of the experiment was to find out what happens in the brain just before the person felt the decision was made. The experiment consisted of wires connected to a person’s brain, to find out how long a person took to press a button. There was a clock and a button, and the people were told to press the button when they felt like it. The experimenters detected some activity in the motor part of the brain;

The second experiment run by Rau, Decola, & Fanselow addresses this interpretation and extinguishes the rats to Context A after they receive the pre-exposure treatment. The results show three important aspects of the enhancement of fear learning by past traumatic events. First, it shows that enhancement is prolonged and lasts at least 7 days after the trauma. The second is that it is obstinate to extinction treatment, even after being safely exposed to where the trauma occurred the effects of the trauma were not changed. Lastly, the results indicated that the enhancement in fear conditioning is not dependent on the current level of fear of the trauma. One of the potential issues with experiment 2 is that it is possible that the enhancement of fear observed in the second context is a summation of new fear-conditioned by the single shock and generalization of reinstated fear of the original traumatic context (Rau et al.,

A few years ago I had to get my blood drawn for the first time. I have always had a fear of needles, so I was not looking forward to having this done. Going into the doctor’s office I was very nervous, my heart was racing. Even during the process of getting my blood drawn I was extremely nervous and uncomfortable. The theory I would apply to this experience is the Cannon-Bard theory. In this theory, the subcortical brain activity in the amygdala leads to both the conscious feeling and the autonomic arousal. In this case, the amygdala sends signals to the cortex creating the conscious experience of fear. The amygdala simultaneous signals to the automatic nervous system creating the intuitive arousal of my heat racing.

I really enjoyed your take on this week’s discussion post and how you approached it primarily from the emotional and biological perspective. As you mentioned, any damage to amygdala can cause a variety of symptoms, but primarily, the individual will experience an impaired ability to practice and/or identify both fear and negative emotions. Individuals with traumatic brain injuries involving the amygdala react differently to various stimuli, mainly due the numerous factors involved in the way that the amygdala responds based on both the location and the level of brain damage sustained. In some, conditions like Kluver-Bucy Syndrome can appear, where the individual has trouble understanding visual information such as mood or facial expressions

First off, one of the biological factors that seemed important was the volume of the amygdala. The amygdala is a section of the brain that is responsible for detecting fear, preparing for emergencies and the controlling of aggression. According to Pardini, Raine, Erickson and Loeber (2015), “men with lower amygdala volumes exhibit higher levels of aggression from childhood to adulthood”. A longitudinal study was done with 56 men who were chosen from 503 males, Caucasian (40.6%) and African-American (55.7%) because of their history with violence . A lower amygdala volume remained constant over the 22-year study, which resulted in higher aggressive and violent behaviours. The study also predicts that in the future that men have an increased

Typically the amygdala is involved in the normal function of interpreting and displaying emotions, memory and fear-conditioning. The amygdala has been found to impact encoding and storage of memories in the hippocampus that are formed during emotional situations. Through such, the hippocampus forms episodic memories based on the amygdala’s interpretation of a particular event and any surrounding emotional stimuli. The ability to properly form memories, experience fear in appropriate situations, and understand and express emotions is critical for an individual to function in society and uphold tenets of the social contract which prevent most people from committing crime.