Fst Stress Theory

This assignment will explore the concept of stress by firstly distinguishing between the definitions set out by Selye 919560 and Cox (1976). Following this assignment will critically evaluate the General Adaption Syndrome, SRRS and Daily Hassles explanations of stress and finally, conclude with a discussion on individual differences based on Friedman and Rosenman’s research.

The cerebral cortex directs functions like speech, behavior, reactions, movement, thinking, and learning. In fact, some research suggests that bipolar disorder originates with problems with the thalamus, which links sensory input to good and bad feelings. The hippocampus also affects depression. It, like the amygdala, is part of the limbic system. It is vital in processing long-term memory. This section of the brain registers recurring fear. In people with clinical depression, the hippocampus is much smaller. Research suggests, even, that ongoing exposure to stress impairs the growth of nerve cells in this part of the brain. One of the most important jobs of the brain is to process senses, through neurons. Neurotransmitters are specific substances that help relay information to the brain. Scientists have identified many neurotransmitters that affect depression. A lack or excess of the neurotransmitters acetylcholine, serotonin, norepinephrine, dopamine, glutamate, lithium carbonate and gamma-aminobutyric acid are thought to contribute to depression. Acetylcholine is involved in learning and enhances memory. Serotonin helps regulate sleep, appetite, and mood, and inhibits pain. Research shows the idea that many depressed people have reduced levels of serotonin. Low levels of a byproduct of serotonin have been linked to a high risk for suicide. Norepinephrine is a neurotransmitter which constricts blood vessels and raises blood pressure. An excess in

stress hormones, it inhibits the growth of nerve cells in this part of the brain. In these depressed

Other clinical studies have implicated fluoxetine’s effects on serotonin neurotransmitters, based on the fact that serotonin is synthesized from the essential amino acid tryptophan. Patients taking fluoxetine who were in remission from major depression were given a special diet which was tryptophan-free. This rapidly decreased plasma serotonin levels, and after a short period of time (as little as 30 minutes) many of the patients began to have signs of specific depressive symptoms. Later, the reappearance of more general depressive symptoms were observed in a majority of the patients. Thus it was shown that fluoxetine has a profound effect on the neurotransmitter serotonin, and decreased

This affects the the brain-derived neurotrophic factor (BDNF)- a crucial factor in the neurobiology of depression. The hippocampus is rich in BDNF, which is related in neuronal growth, survival and maturation, as well as arborization and synaptic plasticity in the adult brain. Stress suppresses BDNF synthesis in the hippocampus showing low concentrations in depressed patients, correlating with the severity of the depression. The use of antidepressant drugs increase its synthesis and signalling in the hippocampus and PFC. In a post-mortem study of depressed patients at the time of death, there were significant differences between the BDNF concentrations in treated and untreated patients. Antidepressants work by balancing neurotransmitters that affect mood and emotion. The use of antidepressants and going to therapy are the most effective ways to treating depression. Weight gain and the feeling of mental numbness is a side effect of antidepressants. Depression can be prevented. Daily exercise, having strong relationships,and watching alcohol intake are ways to prevent depression. Depression is a long term,recurrent condition often taking a chronic course. It is associated with significant morbidity, comorbidity and mortality (suicide and physical illness). In order to achieve and maintain optimum brain function and reduce the risk of recurrence, antidepressant drug treatment full remission is

three groups.Monoamine oxidase inhibitor (MAOI) medicines block the monoamine oxidase enzyme (MAO) from destroying monoamine neurotransmitters, which allows them to accumulate, alleviating depression. Serotonin selective reuptake inhibitor (SSRI) medications block the serotonin reuptake pump, allowing the serotonin neurotransmitter to remain and accumulate in the receptor for longer. Speaking of serotonin specifically, depression has been related to a deficiency of the 5-hydroxytryptamine (serotonin) neurotransmitter as evidenced by the concentrations of the

The physiological and behavioral effects of early life stress (ELS) on the developing and adult brain are a subject of great interest in the field of neuroscience today. The ability to delineate the mechanisms and structures that are affected during postnatal exposure to chronic stress has the potential to provide invaluable insight into the development of a multitude of neuropsychiatric disorders. While we have come to understand a few of the mechanisms involved in many of these illnesses – such as the significance of the serotonin (5-hydroxytryptamine, 5-HT) neurotransmitter in many depression cases – the complex nature of these disorders and our ability to effectively treat them remains elusive. Such an understanding of how the brain adapts and differentially develops as a result of chronic stress, particularly in early life, may also be able to broaden our understanding of the way in which the brain codes and responds to a variety of emotional triggers.

Some studies have considered how the gene for a specific serotonin transporter can play a role in susceptibility to depression. Serotonin is a chemical important in balancing moods, and so it is believed that a deficiency in serotonin may be a cause for depression (McIntosh, 2015). The predictive role of serotonin in depression is exemplified by the monoamine hypothesis that biologically depression is due to lower levels of serotonin (Eley et al., 2010; McIntosh, 2015). For this reason, researchers have studied the effects that a serotonin gene transporter can have on depression

The rats which were depressed were lethargic and lacked survival instincts when tested however with therapy in the form of a rat sized playground they began to show signs of recovery within a month despite their genes. This experiment was also reversed to try to cause depression and was successful “the stressed control rats displayed depressed behaviors when placed in a tank of water. They simply floated- despair behavior- and didn’t try to escape”(3). The science is improving nevertheless humans are complex creatures and hard to study; the experiments conducted on rats cannot be replicated in humans therefore the research has to take a path of observation and

This theory postulates that insufficient activity of monoamine neurotransmitters (serotonin, dopamine, norepinephrine) is the primary cause of depression (Carlson, 2005). This hypothesis is based on experimental findings of increased monoamine oxidase enzyme activity in depressed individuals (Brigatta, 2002). In other words, elevated levels of these neurotransmitters in the brain have all been shown to be effective in the alleviation of depressive symptoms.

In studies that examine serotonin and norepinephrine (NE) it is observed that the concentrations of these chemicals are lower than normal in depressive states. This may point to a deficiency in the concentration of monoamines, which are the chemical precursors to neurotransmitters. Enzymes that control the synthesis and breakdown of neurotransmitters may also play a role in depression. For example, the inhibition of tyrosine hydroxylase, which synthesizes NE, leads to decreased concentrations of NE in the synapse. Furthermore, decreased levels of monoamines and enzyme deficiencies, defects in neurotransmitter receptors on post-synaptic membranes may lead to depression. The signal-cascade pathway that occurs after a neurotransmitter binds to its receptor may be affected at the G-proteins on the surface of the neuron, the cAMP pathway, and protein

The physiological function of each receptor subtype has not been established and is currently the subject of intensive investigation (1).

Synaptic activity is vital for the passage of information throughout the nervous system, as it allows for electrical impulses to be passed from one neuron to another. Electrical impulses in the form of action potentials are passed through the axon of a neuron towards the axon terminal. This information is then passed across the synaptic cleft to receptors present on the postsynaptic membrane via the process of neurotransmission. Drugs can interrupt this specific process in a variety of ways such as through affecting the production, storage and release of neurotransmitters, the presynaptic and postsynaptic receptors as well as the reuptake and destruction of neurotransmitters (Carlson, 2014). Selective Serotonin Reuptake Inhibitors (SSRIs) and Monoamine Oxidase Inhibitors (MAOIs) are just two types of drugs which can affect different pathways in this process of neurotransmission. In doing so, the neurotransmitter serotonin is made more available within the central nervous system (CNS), a neurotransmitter believed to be central to the affective disorder of depression, which is caused by a deficiency of serotonin.

The study of the biochemistry of depression in adults has highlighted the role of neurotransmitters such as norepinephrine, serotonin, and acetylcholine. Research on the biological aspects of depression suggests that during the earlier developmental periods of childhood and adolescence, the neuroregulatory system is not equivalent to that in adulthood. Thus, while many workers still find evidence for a biological dysfunction in childhood depression, a translation of the adult findings would not be sufficient. Most of the characteristics of adult depression are not present with childhood depression, and vise versa.

Neurotransmitters involved in depression include norepinephrine, dopamine, and serotonin. An imbalance of hormones may also play a role in depression. Many depressed people have higher than normal levels of hydrocortisone, a hormone secreted by the adrenal gland in response to stress. In addition, an underactive or overactive thyroid gland can lead to depression.4