PSY396H1 Study Guide - Final Guide: Nmda Receptor Antagonist, Biology Of Depression, Monoamine Oxidase
Document Summary
Sedative-hypnotic drugs cns depressants, gabaa receptor enhancement, more cl conductance. Affective disorders = major depression + bipolar disorder. Major depression = reactive depression or pathological depression. Adoption studies twin studies, monozygotic same vs. different environment, or dizygotic. Neurochemical models of depression = monoamine hypothesis, serotonin dysregulation hypothesis, serotonin-norepinephrine hypothesis. Biological models of depression = glucocorticoid hypothesis, neurotropic hypothesis. Reserpine blocks vmat, vesicular monoamine transporter of monoamines (da, ne, 5-ht) [more nt in cytoplasm mao breakdown less nt in synapse] Cocaine, amphetamine block reuptake of monoamines, increase monoamines, cause mania. Monoamine hypothesis reserpine caused depression because of blocking monoamines, cocaine & amphetamine cause mania by enhancing, but depression onset slow and monoamine levels change fast. Serotonin dysregulation hypothesis measure 5-ht levels in depressed patients, (1) low 5-hiaa. Modulates serotonin activity, higher in tap-water = less suicide-rates (2) ne neurons from locus coeruleus (lc) and 5-ht neurons from raphe nuclei both in brain stem, modulate each other, are functionally and structurally connected.
