PSY 351LEC Lecture Notes - Lecture 22: Nmda Receptor, Ketamine, Cortisol
22 May 2019
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Your sample may include people who do not have depression at all. Etiology hypotheses(cause of depression) :decreased of monoamine in the brain imipramine/reserpine affect depression elevate serotonin or norepinephrine. The cause of depression: too little norepinephrine, serotonin, or dopamine. Treat depression is to fix stress (cortisol) Every morning we wake up have high stress (cortisol)(glucocorticoid) hypothalamus-->pituitary gland acth adrenal cortex--> cortisol (include negative feedback send to hypothalamus)(poor) Dst: test negative feedback, fail= stress still there (fail suppress, block) (negative feedback is not working) ---> depression. Depression patients have higher glucocorticoid, because negative feedback do not work. People have history of depression have more crh/crf neurons. Treatment anti depression drug enhance negative feedback. Patients who have depression have high blood glutamate. Nmda glutamate around it open, we cell active(depolarization) mg gone, when cell rest.
