Autonomy

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Department
Biological Sciences
Course
BIOC31H3
Professor
Malcolm Mac Kinnon
Semester
Fall

Description
This tendency was especially evident among people high in autonomy. Depression and martial discord frequently co-occur. Constant seeking of reassurance is a critical variable in depression. Even when reassured, they are only temporarily satisfied. Their negative self-concept causes them to doubt the truth o the feedback they have received, and their constant efforts to be reassured come to irritate others. Social skills deficits may be a cause and consequence of depression. PSYCHOLOGICAL THEORIES OF BIPOLAR DISORDER: patients with bipolar depression have elevated levels of the dysfunctional attitudes described by Beck, as well as problems in autobiographical memory and the ability to generate solutions in problem- solving task. The manic phase of the disorder is seen as a defence against a debilitating psychological state. BIOLOGICAL THEORIES OF MOOD DISORDERS: THE GENETIC DATA: bipolar disorder is one of the mot heritable of disorders. Genes account for possibly 85% of variance in whether a person becomes manic. th Evidence favouring the hypothesis that bipolar disorder results from a dominant gene on the 11 chromosome. Within bipolar disorder, variation in the brain-derived neurotrophic factor (BDNF) gene appears to predict risk for developing rapid cycling. Some people seem to be genetically predisposed to the onset of MDD when confronted with a series of adverse life-events. Serotonin transporter gene-linked promoter region (5-HTTLPR), which is involved in modulating serotonin levels, is a significant predictor of first major depression onset following multiple adverse events. NEUROCHEMISTRY, NEUROIMAGING AND MOOD DISORDERS: The original theory posited that low levels of norepinephrine and dopamine lead to depression and high levels to mania. The serotonin theory suggests that serotonin, a neurotransmitter presumed to play a role in the regulation of norepinephrine, also produces depression and mania. However, the weight of the evidence does not completely support the notion that levels of neurotransmitters are critical in the mood disorders. Tricylclic drugs: i.e. imipramine, or Tofranil are group of antidepressant medications so named because their molecular structure is characterized by three fused rings. They prevent some of the reuptake of norepinephrine, serotonin and or dopamine by the presynaptic neuron after it has fired, leaving more of the neurotransmitter in the synapse so that transmission of the next nerve impulse is made easier. Monoamine oxidase (MAO) inhibitors: I.e. Tranylcypromine or Parnate are antidepressant drugs that keep the enzyme MAO from deactivating neurotransmitters, thus increasing the levels of serotonin, norepinephrine and or dopamine in the synapse. This action produces the same facilitating effect decried for tricylics, compensating for the abnormally low levels of these neurotransmitters in depressed people. Newer antidepressants, called selective serotonin reuptake inhibitors, i.e fluoxetine or Prozac, act more selectivel, specifically inhibiting the reuptake of serotonin. It now appears that the explanation of why these drugs work is not as straightforward as it seemed at first. Both tricyclics and MAO inhibitors take from seven to 14 days to relieve depression, but by that time, the neurotransmitter level has already returned to its previous state. Another approach to further evaluate the theories involved measuring metabolites of these NT, the by-products of the breakdown of serotonin, norepinephrine, and or dopamine found in urine, blood serum, and the cerebrospinal fluid. The problem with such measurements is that they are not direct reflections of levels of NT in the brain; metabolites measured in this way could reflect NT anywhere in the body. Further, the expected high or low metabolites were not found consistently, thus, many people with depression or mania did not have disturbances in absolute levels of NT. It would seem, then, that a simple change in the level of norepinephrine or serotonin or dopamine is not a sufficient explanation for why people become depressed and/or manic. One lin
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