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Biology of obsessive–compulsive disorder : ウィキペディア英語版
Biology of obsessive–compulsive disorder

The biology of obsessive–compulsive disorder primarily involves the brain regions of the striatum, the orbitofrontal cortex and the cingulate cortex. People with OCD evince increased grey matter volumes in bilateral lenticular nuclei, extending to the caudate nuclei, while decreased grey matter volumes in bilateral dorsal medial frontal/anterior cingulate gyri.〔
〕 These findings contrast with those in people with other anxiety disorders, who evince decreased (rather than increased) grey matter volumes in bilateral lenticular / caudate nuclei, while also decreased grey matter volumes in bilateral dorsal medial frontal/anterior cingulate gyri.〔 OCD involves several different receptors, mostly H2, M4, NK1, NMDA, and non-NMDA glutamate receptors. The receptors 5-HT1D, 5-HT2C, and the μ opioid receptor exert a secondary effect. The H2, M4, NK1, and non-NMDA glutamate receptors are active in the striatum, whereas the NMDA receptors are active in the cingulate cortex.
==Receptors==
The activity of certain receptors is positively correlated to the severity of OCD, whereas the activity of certain other receptors is negatively correlated to the severity of OCD. Activity of the histamine receptor (H2); the Muscarinic acetylcholine receptor(M4); the Tachykinin receptor (NK1); and non-NMDA glutamate receptors are positively correlated with symptom severity in OCD. Associations for which activity is negatively correlated with severity include the NMDA receptor (NMDA); the Mu opioid receptor (μ opioid); and two types of 5-HT receptors (5-HT1D and 5-HT2C). The central dysfunction of OCD may involve the receptors nk1, non-NMDA glutamate receptors, and NMDA, whereas the other receptors could simply exert secondary modulatory effects.

抄文引用元・出典: フリー百科事典『 ウィキペディア(Wikipedia)
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