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KMID : 0385620010100020097
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Korean Journal of Psychopathology
2001 Volume.10 No. 2 p.97 ~ p.103
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Molecular and Cellular Hypothesis of Antidepressant Action
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Abstract
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Recent studies have resulted in considerable advancement of the monoamine hypothesis of mood disorder. Whereas earlier models focused on alternations in synaptic levels of monoamines such as serotonin and norepinephrine, more recent studies
demonstrate
a major role for neural placidity in the etiology and treatment of depression. Several basic and clinical studies have provided direct evidence of neuronal atrophy and loss in response to stress and depression. Stress can result in atrophy and
death of
CA3 pyramidal neurons and decrease the neurogenesis of dentate gyrus granular neurons in the hippocampus of adult animal. Recent studies also demonstrate that antidepressant treatment upregulate the cAMP-CREB cascade and expression of BDNF.
Upregulation
of CREB and BDNF raises the possibility that antidepressant treatment could oppose the cell death pathway. Recent studies also demonstrate that chronic antidepressant treatment increases the neurogenesis of dentate gyrus granular cells. These
findings
raise the possibility that increased cell proliferation and neuronal number may be a mechanism by which antidepressant treatment overcomes the stress-induced atrophy and loss of neurons in the hippocampus and may contribute to the therapeutic
actions of
antidepressant treatment.
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KEYWORD
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