Amygdala In The Brain Analysis

This analysis persists of key points, about The article “Stress and the brain by Janet Elder”. The author forged an excellent informative piece to educate the reader on the effects of stress on the brain. The author states that “Stress can be both good and bad. It is part of life, and your brain and body respond to it”. The author clarifies that, "Whether stress is harmful or helpful depends on the amount of stress, how severe it is, and how long it lasts".

“The ‘stress hormone’ cortisol is believed to create a domino effect that hard-wires pathways between the hippocampus and amygdala in a way that might create a vicious cycle by creating a brain that becomes predisposed to be in a constant state of fight-or-flight” (Bergland, 2014).

.) As Dr. Perry states, “the stress response system originates in the lower parts of the brain and help regulate and organize higher parts of the brain; if they are poorly organized or regulated themselves, they dysregulate and disorganized higher parts of the brain”

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

(2) However, there are some problems with this evidense. Amphetamines only mimic the positive symptoms of schizophrenia. They do not produce any of the negative symptoms. Likewise, anti-psychotic drugs are only affective on the positive symptoms of the disease. There is still some evidense that schizophrenics do posess higher levels of dopamine, however, these increases are only found in the striatum of the brain (7). The striatum is a region of the brain that receives its inputs from and outputs to the cortex. Injury to the striatum results in problems with intiation and control of motor behavior. (9) Also, there is evidence that the prefrontal cortex produces lower levels of dopamine. (4) The prefrontal cortex is involved in the organization and coordination of information to and from the cortex. (7)

Researchers think that overly responsive dopamine systems might magnify brain activity in some way, perhaps creating hallucinations and other so-called positive symptoms as the brain loses its capacity to tell the difference between internal and external stimuli. For this reason, dopamine blocking drugs are often used as anti-psychotic medications in treatment. Modern neuroimaging studies show that some people with schizophrenia have abnormal brain activity in the thalamus,when patients were hallucinating for example, which is involved in filtering incoming sensory signals. Patients with paranoid symptoms showed over-activity in the fear processing amygdala. Schizophrenia seems to involve not just problems with one part of the brain, but abnormalities in several areas and their interconnections. What might be causing these abnormalities under the “iathesis-stress” model? This way of thinking involves a combination of biological and genetic vulnerabilities -diathesis- and environmental stressors -stress- that both contribute to the onset of schizophrenia. This model helps explain why some people with genetic vulnerability might not always develop schizophrenia and why the rates of schizophrenia tend to be higher with some degree of poverty or socioeconomic stress. It seems too that there is some kind of genetic predisposition for the

Dopamine is a neurotransmitter associated with attention. Schizophrenics seem to have an increased number of D2 dopamine receptors on receiving neurons. This theory is support by the fact that Phenothiazines bind with D2 receptors and reduce positive symptoms. Another piece of supporting evidence is that Parkinson’s disease drug L-dopa, increase the level of dopamine and causes schizophrenic like symptoms in some people. However excess dopamine can only explain some types of schizophrenia, usually positive rather than negative.

Over the years, experiments have produced evidence to suggest that dopamine plays a role in the development of Schizophrenia (Howes, McCutcheon, & Stone, 2015). Dopamine is a neurotransmitter that is produced in the substantia nigra and ventral tegmental regions of the brain. The belief that dopamine was involved in Schizophrenia arose after multiple studies performed with compounds produced an increase in extracellular concentrations of dopamine (Lieberman, Kane, & Alvir, 1987). The patients that were administered these compounds had similar symptoms to those observed from patients who were diagnosed with Schizophrenia (Lieberman et al., 1987).

The term ‘amygdala’ was first used by Burdach (1819) and referred to a set of nuclei in the brain (Aggleton & Saunders, 2000). In 1939, researchers Klüver & Bucy inflicted bilateral lesions of the inferior temporal lobe of monkeys in a laboratory in an attempt to reduce aggression. These lesions affected the cortical areas, amygdala, and the hippocampus. Later this became known as Klüver-Bucy syndrome, and consisted of symptoms such as psychic blindness, hypermetamorphsis, oral tendencies, and changes in emotional and sexual behaviors. Lesions of the amygdala made monkeys fearless of e.g. humans or snakes, and affectively flat, tame. This research brought recognition to the notion that the amygdala plays a significant role in the

The Dopamine Model (DM) has been around since the twentieth century (Preston, O’Neal and Talaga, 2017). The model believes that the cause of schizophrenia symptoms is from abnormal dopamine in the brain (Preston, et al., 2017). The premise is based off two observations. The first one is that antipsychotic drugs are able to bind and block the dopamine receptors (Preston, O’Neal, et al., 2017). The second observation is that the antipsychotic drugs increases dopamine which create paranoid schizophrenia symptoms (Preston, et al., 2017).

The adult brain is described as the brain to think by feeling. We are feeling machines that think. Hardships that effect the brain can be post-traumatic stress disorder (PTSD), depression, and stroke. The brain reacts in different ways, especially in the adult brain. When the brain encounters a stroke, it cannot process emotions because there are no neurons functioning. Generally, when the brain encounters an emotional event, the amygdala is the first brain structure to respond. The role of the amygdala and the brain stem when responding to an emotional event is working together to get a response through the body. The nerve impulse travels from the amygdala down the brain stem; without each other, the body would not function right. Although

Hughes & Baylin (2012) place importance on a parent being able to read their children’s expression and non verbal cues in order to stay close to their children and to experience parenting as rewarding. “The parenting child -reading system is fundamental to the process of attuning to a child’s inner states, to creating the kind of intersubjective, mind to mind communication” (Hughes & Baylin, 2012, p. 71). The amygdala plays a central role in this parenting system by supporting the parent to make a quick perception of the child’s communication as either positive or negative. If the amygdala detects a threat, the parents defence system is set off and could suppress parental curiosity and reflection and promote a defensive reaction to the child which the child then has to respond to.

This article provides information as to how the brain historically has used dopamine as an inhibitory neurotransmitter in regards to schizophrenia. The research discussed in this article focuses on a new discovery that indicates that glutamate, GABA, acetylcholine and serotonin alterations are also involved with schizophrenia’s pathology. With use of schizophrenic animal models, both dopamine receptors and the antipsychotic effects of the treatments that target them, and how they interact with other various neurochemical types of schizophrenia. The final topic the author discusses is how the human brain and mental abilities has evolved, causing many schizophrenic patients to be affected.

The purpose of the present study is to evaluate how people with bilateral amygdala damage compare, in terms of both visual and physiological differences, when exposed to varying amounts of Carbon Dioxide gas. The researchers noted that they observed behavior changes, change in vital signs (such as heart rate, respiration rate, etc.) to compare panic levels in: people with no amygdala lesion, people with an amygdala lesion, and a comparison control group that was not exposed to panic-inducing stimuli. The researchers specifically chose individuals with amygdala damage/lesion(s), as prior research as indicated a correlation between the amygdala’s function and elicited anxiety, anger and/or panic. In an initial study, a comparison group exposed

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.