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- W2372654737 abstract "Post-traumatic stress disorder (PTSD) is an anxiety disorder that can develop after exposure to one or more traumatic events threatened or caused grave physical harm. Amygdala nucleus is the brain's center and links closely with the traumatic memories and activation of hypothalamic-pituitary-adrenal(HPA) axis under stress. PTSD patients have a strong sense of fear and startle response, abnormal low blood glucocorticoid concentration, disordered HPA axis. Amygdala regulates the HPA axis through the activation of glucocorticoid receptor(GR) and mineralocorticoid receptor(MR), and increases the release of glucocorticoid. PTSD induces the apoptosis of amygdala neurons regulated by apoptotic related genes Bax and Bcl-2 with the increase of Bax/Bc-2 ratio. PTSD induces long-term potentiation (LTP) in amygdala neurons which are the key hub of the conformation and express of fear, LTP is a neurophysiological basis of learning and memory. In the conformation of conditioned fear, the occurrence of LTP indicates that LTP is an important indicator of the mechanism of PTSD. PTSD causes the decrease of activity of acetylcholinesterase (AChE), the increase of acetylcholine, enhancement of fear. PTSD changes the expression of MR, GR and MR/GR in amygdala neurons, activates HPA axis, resultes in the disturbance of HPA axis. The amygdala is closely linked with PTSD and may play an important role in the pathogenesis of PTSD." @default.
- W2372654737 created "2016-06-24" @default.
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- W2372654737 date "2009-01-01" @default.
- W2372654737 modified "2023-09-25" @default.
- W2372654737 title "The Relationship of Amygdala Nucleus with Pathogenesis of Post-traumatic Stress Disorder" @default.
- W2372654737 hasPublicationYear "2009" @default.
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