大脑神经可塑性与情绪障碍的治疗.pptxVIP

Treating emotional disorders with neuroplasticity in mind 大脑神经可塑性与情绪障碍的治疗;Part I: Basics about neuron 第1部分：神经元基础知识;Dendrite, Axon, and Synapse 树突, 轴突和突触;Dendritic length and dendritic spines 树突长度和树突刺;Receptors along dendrite: genetic potential vs actual expression 受体数量：遗传可能数量 对 实际数量 ;Factors that affect dendritic length, spines density, and actual numbers of receptors影响树突长度, 树突刺密度, 和实际受体数量的因素;Part II: Basics about neuroplasticity 第2部分：神经可塑性基础知识 ;“Cells that fire together, wire together.” (Hebb, 1949);Experience-induced dendritic growth or shrinkage (Trachtenberg et al, 2002) 经验诱导的树突增长或缩短;(2) Experience-induced changes in spines density (Kolb et al., 2003) 经验诱导的树突刺密度改变;(3) Experience-induced changes in synaptic efficiency (Kandel, 2001) 经验诱导的突触功效改变;(4) Experience-induced cortical reorganization (Merzenich et al., 1984)经验引起的皮层重组;(5) Chronic stress, elevated cortisol, suppressed neurogenesis and shrunk hippocampus 长期压力, 皮质醇升高, 抑制神经元形成, 海马萎缩 (Gould Tanapat, 1999) ;(6) Learning and practices also create angiogenesis (Holloway,2003) 学习和实践还可以引起血管生成;(7) Emotional experience induces changes in the peptile systems (Pert, 1997)情感性经验引起生物肽系统的改变; Part III: How does emotional dysregulation lead to dysregulated brain? 第3部分：情绪失调怎样导致大脑失调;Dual-process model of emotion regulation (LeDoux,1996)情绪调节的双轨模式;Immediate threat and the ANS 直接威胁与自主神经系统;The immediate threat alarm直接威胁警报;Negative emotions and somatic symptoms 负性情感与躯体化症状;What happen if threats persist? 如果威胁持续会怎样？;Chronic threat and the HPA慢性威胁与HPA (下丘脑－垂体－肾上腺轴);The long-term struggle alarm 长期战斗警报;Cortisol suppresses peptides and proteins synthesis in our body. Neurotransmitters, neurons, enzymes, body cells and antibodies are all either amino acids, peptides or proteins. Long term suppression of peptides or proteins synthesis can lead to their deficiencies and the associated mental and physical problems 皮质醇抑制体内生物肽和蛋白质的合成。神经递质，神经元，酶，体细胞和抗体都是氨基酸，多肽或蛋白质的合成物。长期抑制多肽和蛋白质合成会导致这些物质的