주요우울증에서 사이토카인-세로토닌 상호작용에 의한 신경변성 가설A Neurodegenerative Hypothesis of Cytokine-Serotonin Interaction in Major Depression
- Other Titles
- A Neurodegenerative Hypothesis of Cytokine-Serotonin Interaction in Major Depression
- Authors
- 김용구
- Issue Date
- Jul-2004
- Publisher
- 대한신경정신의학회
- Keywords
- Serotonin; Cytokine; Neurogenesis; Neurodegeneration; IDO; Depression; 세로토닌; 사이토카인; 신경조직발생; 신경변성; 우울증.
- Citation
- 신경정신의학, v.43, no.4, pp 386 - 392
- Pages
- 7
- Indexed
- KCICANDI
- Journal Title
- 신경정신의학
- Volume
- 43
- Number
- 4
- Start Page
- 386
- End Page
- 392
- URI
- https://scholarworks.korea.ac.kr/kumedicine/handle/2020.sw.kumedicine/32204
- ISSN
- 1015-4817
- Abstract
- A growing body of evidence suggests that major depression is associated with increased productions of pro-inflammatory
cytokines such as IL-1, IL-6, IL-12 or TNF-alpha and increased concentrations of prostaglandin E2 and negative-regulatory
cytokines such as IL-4 or IL-10. In major depression, interactions among brain 5-HT levels, the activity of its autoreceptors,
and that of postsynaptic receptors play a critical role in mood changes and depression. Recently, the link between cytokines
and serotonergic turnover has been explored. Cytokines such as IL-1, IL-2 and IFN-gamma reduce the production of 5-HT by
stimulating the activity of indoleamine-2,3 dioxygenase (IDO), an enzyme which convert tryptophan, the precursor of 5-HT to
kynurenine. The kynurenine is metabolized into quinolinic acid (quinolinate) and kynurenic acid (kynurenate), an excitotoxic
NMDA receptor agonist and the antagonist of three ionotropic excitotatory aminoacid receptors, respectively. The cytokineserotonin
interaction through IDO that leads to the challenge between quinolinate and kynurenate in the brain may finally
induce the neurodegeneration in depression. The neurodegeneration hypothesis of depression can explain how people cope
with psychological or physical stress at different stages according to severity and duration of stress and why major
depression develops. (J Korean Neuropsychiatr Assoc 2004;43(4):386-392)
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