[생리심리] Neurobiology of Depression(영문)
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추천 연관자료
- 목차
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Table of contents
1. Danger of depression
2. Diagnosis and symptoms of depression
3. Causes
A. General
i. Neurotransmitter
ii. Genetic and Nongenetic
B. Neural circuitry
i. Stress
ii. BDNF
4. Treatments
- 본문내용
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b. Genetics
In researches about genetic factor,strong geneticrisk modifierhas not been discovered. Some researches have been conducted, but their results conflicts, and they are difficult to retest. Moreover, even if research has been conducted, the same results seldom occur.
c. Nongenetics
As nongenetic factors, there are stress, emotional trauma and viral infections. One famous example is Borna virus, a viral infection of farm animals. Animals with this virus show frantic activity alternating with periods of inactivity, which symptom is similar to bipolar disorder. Emotional trauma is another cause of depression. People who experienced rape, physical abuse are more prone to suffer from depression. Numerous theories exist, but the fact that stress is one of the main causes is generally accepted. This can be explained by observing HPA axis and cortisol showed below.
-Neural circuitry
a.stress
The CRH (Corticotropin-releasing hormone) neurons of the Hypothalamus are controlled by two structures: the amygdale and hippocampus. The amygdale has significant role for fear responses. Sensory information enters the basolateral amygdale, where it is processed and relayed to neurons in the central nucleus. When the central nucleus of the amygdale becomes active, the stress response ensues. Inappropriate activation of the amygdale, as measured using functional magnetic resonance imaging, has been associated with some anxiety disorders. Under the amygdale is a collection of neurons called the bed nucleus of the stria terminalis. The bed nucleus neurons activate the HPA axis and the stress response.
The HPA axis is also regulated by the hippocampus. Hippocampal activation suppresses CRH release. The hippocampus contains numerous glucocoticoid receptors that respond to the cortisol released from the adrenal gland response to HPA system activation. Thus, the hippocampus normally participates in the feedback regulation of the HPA axus by inhibiting CRH release and the subsequent release of ACTH and cortisol when circulating cortisol levels get too high. Continuous exposure to cortisol, however, as occurs during periods of chronic stress, can cause hippocampal neurons to wither and die in experimental animals. This degeneration of the hippocampus sets off a vicious cycle in which the stress response becomes more pronounced, leading to even greater cortisol release and more hippocampal damage. Human brain imaging studies have posttraumatic stress disorder, an anxiety disorder that is triggered by exposure to inescapable stress.
b.BDNF
Neurotrophinsand neurogenesis.
Volumetric decreases observed in the hippocampus and other fore brain regions in subsets of depressed patients have supported a popular hypothesis for depression involving decrements in neurotrophic factors – neurodevelopmentally expressed growth factors that also regulate plasticity within adult brain. From a serial of depression patients’ decreased volume of hippocampus and other prefrontal region was observed. This supports popular hypothesis including decrease of neurotrophic factors. Neurotrophic factors are growth factors which acts neurodevelopmental role and mediates plasticity within adult brain. These studies have focused largely on the role of brain-derived neurotrophic factor (BDNF), which is expressed abundantly in adult limbic structures. Support for this ‘BDNF hypothesis’ has come from a large preclinical literature showing that several forms of stress reduce BDNF-mediated signaling in the hippocampus, whereas chronic treatment with antidepressants increases BDNF-mediated signaling. BDNF hypothesis, which came from support of many studies, states about the ways stress reduces BDNF-mediated signaling in hippocampus. On the other hand, sustained treatment of anti-depressant shows increase of BDNF-mediated signaling. Similar changes have been observed in the post-mortem hippocampus of humans with depression, as well as in the concentrations of serum BDNF, the source of which remains controversial. Similar changes were observed in the hippocampus of depression patients, and the role of level of BDNF-mediated signaling is still being discussed.
More causal evidence for the antidepressant action of BDNF has come from experiments in rodents in which antidepressant effects were observed on direct infusion of BDNF into the hippocampus and were blocked on the conditional or inducible knockout of the gene encoding BDNF from forebrain regions. The more supportive study of antidepressants’ activity on BDNF level was done through experiments using rats. In order for the Researchers to observe the direct effect on BDNF in hippocampus of the rats, they observed the gene encoding of the rats’ frontal lobes blocking the BDNF by blacking out the rats. However, more recent findings have necessitated a revision of this hypothesis. First, a substantial number of preclinical studies either have failed to show these patterns of cha
- 참고문헌
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References
구재우, 이화영, 백종우, 강이헌, & 이민수 (2006). 한국인 우울장애 환자에서 Brain-derived
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Depression. National Institute of Mental Health. 30 May, 2011.
http://www.nimh.nih.gov/health/publications/depression/complete-index.shtml#pub10.
Grohol, J. M. (2008). TMS treatment gains FDA approval. Psych Central. 04 June, 2011.
http://psychcentral.com/blog/archives/2008/10/09/tms-treatment-for-depression-gains-fda-approval/.
Nemade, R. Biology of Depression – Neurotransmitter. El Paso Mental Health & Mental
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http://info.epmhmr.org/poc/view_doc.php?type=doc&id=12999&cn=5.
Nestler, E. J., et al. (2002). Neurobiology of Depression. Cell Press. Vol 34.
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