Dosal Raphe Summary

There are three different theories that are used when talking about how we react to stress through the physiological aspect or the psychological aspect. The first is part of the physiological aspect of stress called the Cannon Fight or Flight theory which was proposed in 1914. Fight or Flight response is a physiological stress response that evolved to help organisms to survive immediate danger. The theory states that when an organism, human being or animal, faces imminent danger (acute stressor) the body arouses quickly and is ready to act via two different systems. They are the sympathetic nervous system and the endocrine system. The sympathetic nervous system stimulates the adrenal medulla which is part of the endocrine system and is the region that produces the hormones such as adrenaline and noradrenaline. These hormones increase heart rate, blood flow, and glucose levels to prepare the body for an emergency. This response from the body suggests that the body knows how to protect itself and reach homeostasis. These two systems work together to either fight against the danger or flight away from the danger. Lord, King and Pfister in 1976 studied the Fight or Flight response in animals through a very unethical study. They administered chemicals on male hooded Wistar rats which inhibited the neurotransmitters from functioning normally. This made it very difficult for the rats to escape an electric shock. The results of the study suggest that the Flight or Fight response

A test done by Robert Sapolsky form Stanford University shows how anxiety can escalate to depression through subjecting rats to electric shock. The shocks occurred periodically and the rats soon learned that to stop the shocks, they had to press a lever. Once that was learned, the rats were seen to be constantly alert, waiting for the shocks to occur. However, the next time they occurred, the levers were disable and the rats repeatedly pressed it, hoping the shocks would stop. After a while, they realize that their efforts are futile and went into despair, which is measured through the levels of dopamine, serotonin and noradrenaline (norepinephrine) in their brains. (SCI. AMERICAN)

Pharmacodynamics (PD): DVS prolongs the action of serotonin (5-HT) and noradrenaline (NA) in the central-nervous-system (CNS) by selectively binding to synaptic reuptake transporters.2-4 (See fig 1).5 5-HT and NA are powerful neurotransmitters that regulate mood and mental wellbeing.3

The amygdala is made up of a group of nuclei located in the medial temporal lobe of the brain. (Mannironi, et al., 2013) The amygdala is believed to be key in stress response integration with its extensive network of efferent outcrops to other regions of the brain. (Mannironi, et al., 2013) Stress mediators such as adrenaline, cortisol, and corticotrophin releasing hormone, contribute to neuronal operative change and plasticity that are instrumental contributory to the stress response. (Mannironi, et al., 2013) Acute psychological stress creates a instant surge of hormone release, neuronal activation, and neurotransmission. (Mannironi, et al., 2013) This activation has an intense effect on the brain, leading to structural modification in the synaptic connectivity and dendritic spine morphology. (Mannironi, et al., 2013)

There are numerous neurological changes occurring in our body as a response to fear. Specifically, two pathways are activated: the sympathetic nervous system and the hypothalamic- pituitary- adrenal pathway. In a similar way, both pathways commence by receiving messages from the hypothalamus, an area of the brain responsible for many functions in the body, such as activating the autonomic nervous system, controlling different organs, and managing physiological functions. If the hypothalamus emits messages that we are facing a threatening situation, it will release different chemicals to either the sympathetic nervous system and the hypothalamic- pituitary- adrenal pathway. This sympathetic nervous system are “nerve fibers of the autonomic

Opioids are important for pleasurable experience . If we observe a hedonic spectrum, we sould see, that opioids shift it in positive direction : while sweat tastes seem sweater , bitter tastes and pain seem less aversive. Blocking of opioid-mediated signalling results in decreased pleasantness of rewards. Recent studies have shown, that there is a dissotiation between the way how µ-opioid and κ-opioid – receptor related signalls modulate the perception of pain.( µ and κ come from the name of the first discoverd ligand that attach to this receptors: µ stands for morphine and κ for ketocyclazocine ). The activation of µ-opioid receptors induces

The adrenal medulla is stimulated by the sympathetic nervous system to release norepinephrane and epinephrine in response to stress.

Meyer et al 2014 In vertebrates the stress response is an evolutionary conservative process mediated by the HPA access and allows organisms to respond rapidly to unpredictable changes in their environment. It is initiated when higher brain centers perceived and endogenous or exogenous noxious stimuli that are in homeostasis and how many it’s release of good corticoids from the adrenal cortex. Elevated levels of circulating clinical records exert a variety of catabolic and Terry productive anti-gross and immunosuppressive effects that mobilize and repartition under detailed organisms restore homeostatic balance. Other than physiological response to short-term stress is adaptive long-term stress occurring over weeks to months may lead to pathological syndrome of distress characterized by amino suppressive decreased reproduction and diminish growth. According Lee measures of population performance such as survival for productive output and abundance may be reduced as a proportion of distress individuals it a population increases. . (MacBeth et al. 2010) The hypothalamus pituitary digital access to respond rapidly and specifically to wide range of environmental and internal demand half deferred to her stress. Is believed to HP a response to stress plays a pivotal role in our in his

The article described how pyramidal cells relate to anxiety disorders, while lecture mentioned how pyramidal cells are aligned in schizophrenic patients, in turn affecting their behavior. Lastly, the article stated that the brain produces elevated levels of dopamine in the prefrontal cortex when the brain is under stress. There is also an overproduction of dopamine in schizophrenic patients, which, in turn, produce positive symptoms (Renee, 2017). It is fair to conclude that overproduction of dopamine can have negative consequences on the brain, which is evident in both anxiety disorders and people with schizophrenia. Overall, there were critical differences between the article and the textbook, but the differences stem from differing perspectives on the same brain structure, brain neuron, and brain

Neurotransmitter Systems. The study of monoamines in relation to MDD has been at the forefront for the majority of the time that the subject itself has been under research. With a particular focus on serotonin (but also norepinephrine and dopamine), these studies find that the rate of serotonin synthesis is often low in depressed patients (Rosa-Neto et al., 2004). Interpretation of serotonin levels may however become problematic, because it can be concluded that: depression may cause a low synthesis of serotonin; a low synthesis of serotonin may cause depression; or that another third process may cause both a low synthesis of serotonin and depression simultaneously. There is little doubt that a decrease in serotonin plays a key role in MDD but the notion of whether the neurotransmitter’s absence is a mechanism that is uniquely responsible, or merely a

Neuroscience. When an anxiety response occurs, objectively unthreatening stimuli becomes threatening (Davidson, 2013). To help cope with stress, the brain releases the hormone cortisol (Bear, Connors & Paradiso, 2007). During the fear and anxiety response, the central nucleus of the amygdala is active; once active, an excitatory response in the hypothalamus occurs (Davidson, 2013). This excitation causes corticotrophin-releasing-hormone (CRH) to be released; CRH then triggers the anterior pituitary gland to secrete ACTH (Davidson, 2013). The ACTH levels in the blood stream cause cortisol to be released from the adrenal cortex and once the levels of cortisol become high, the hippocampus activates, suppressing the release of CRH (Davidson, 2013). The bloodstream carries cortisol to the brain, where it bind to receptors in the cytoplasm of man

Serotonin is a neurotransmitter in the brain that has an immense effect over many functions of the brain. “Cells that make serotonin use tryptophan hydroxylase, a chemical reactor which, when combined with tryptophan, forms 5-hydroxytryptamine”. Serotonin can be discovered three key parts of the body. However, the main location of serotonin lies within the intestinal walls. It is also located within large blood vessels throughout the body and the central nervous system. The most commonly studied area of the body when it comes to serotonin, is how this neurotransmitter effects the central nervous system. The functions of serotonin are abundant and can include the regulation of many important attributes of the human body such as appetite, sleep, mood, behavior, endocrine regulation, and depression.

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.

Serotonin (5-hydroxytryptamine, 5-HT) is a neurotransmitter in the brain that has an enormous influence over many brain functions. It is synthesized, from the amino acid L-tryptophan, in brain neurons and stored in vesicles. Serotonin is found in three main areas of the body: the intestinal wall; large constricted blood vessels; and the central nervous system. The most widely studied effects have been those on the central nervous system. The functions of serotonin are numerous and appear to involve control of appetite, sleep, memory and learning, temperature regulation, mood, behavior (including sexual and hallucinogenic behavior), cardiovascular function, muscle contraction, endocrine regulation, and

The two different mental disorders, anxiety and depression, obtain more in relation everyday. Although each can have different causes and characteristics they share many common ones. Strong links throughcertain illnesses and disorders like asthma and headaches are being configured through specific chemicals in the brain. Two examples being serotonin receptors and corticotropin releasing factor receptor1. Certain combinations of the two can lead to a change in energy leveles causing both anxiety and depression to occur at the same time. Many treatments used for both are also the same, this including some antidepressant medicines.