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Moving Beyond the Monoamine Hypothesis to Examine the Fundamental Difference in Endocrine Function between Depressed Patients and Normal Patients and Differences in the Physiological Mechanism

Ahmad, Myra

According to the DSM-IV-TR, a depressive disorder is an “illness that involves the body, mood, and thoughts.” It affects the way a person carries out the necessary functions of life, like eating or sleeping, the way a person feels and thinks about themselves and about the world at large. The most popular neurophysiological theory of depression follows from the drugs that are used to treat it. Monoamine oxidase is produced by all monoamine neurons and functions to dominate these neurotransmitters in the terminal button. Therefore, the amount of monoamine available for storage and release is regulated by MAO. Evidence in support of the Monoamine Hypothesis is that levels of 5- HT, as measured by its metabolites, seem to be correlated with depression. Thus, selective serotonin reuptake inhibitors (SSRIs) were developed specifically to inhibit the reuptake of serotonin by competitively binding without the serotonin transporter protein. Another theory of depression also follows from successful treatment. The fact that sleep deprivation can effectively treat depression has lead some to the conclusion that abnormal sleep patterns may play a role in depression. The final theory of depression addressed the previous theory of depression in that the patients have seen successful results with the effects of sleep deprivation on their depression, but will feel depressive symptoms shortly after a small bout of sleep. These hypotheses all point a fundamental difference in endocrine function between depressed patients and nondepressed patients and suggest differences in the physiological mechanism underlying their endocrine feedback control systems.

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More About This Work

Academic Units
Psychology (Barnard College)
Degree
B.A., Barnard College
Published Here
April 23, 2013
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