The Metabolism of Norepinephrine in Depressions: Differences and Effects of Therapies

Abstract

The metabolism of infused H3-norepinephrine was studied in twenty psychiatric patients with depression. A difference was found in the metabolism in those patients classified as manic-depressive in that they tended to have a definite increase in the urine in the proportion of those metabolites which retain the amine group as compared to the metabolites which had undergone oxidative deamination (N/O ratio). The main amine metabolite was normetanephrine while the main oxidized metabolite was vanillomandelic acid. Patients diagnosed as reactive depression also tended to have an elevated N/O ratio, but to a lesser degree than the manic-depressives. Those patients with involutional psychosis or schizophrenia with depression did not differ from the normals in the amine metabolism. E.C.T. appears to be especially effective in those patients with an abnormal amine pattern and it also corrects the disturbance in the metabolism. Chlorpromazine, imipramine, amitriptyline and chlordiazepoxide cause a marked change in the metabolic pattern of norepinephrine. Evidence is cited which suggests that the altered norepinephrine metabolism may result in an elevation of normetanephrine at synaptic sites which could antagonize the action of sympathetically-released norepinephrine.

Acid hydrolysis followed by matrix‐assisted laser desorption/ionization mass spectrometry for the rapid diagnosis of serum protein biomarkers in patients with major depression

“…Previously, several theories have been proposed for the pathogenesis of this disease, including a chronic and systemic immune activation, the monoamine theory of norepinephrine and serotonin, and regulation of brain‐derived neurotrophic factors (BDNF) and tissue‐type plasminogen activators 1–8. The results of previous studies have shown that a correlation exists between patients with affective disorders and several small biochemical compounds in sera, such as lipids (e.g., total cholesterol and triglyceride), serotonin, norepinephrine, γ ‐aminobutyric acid (GABA), glutamate, insulin‐like growth factor 1, glia maturation factor (GMF‐β), and hippocampal cholinergic neurostimulating peptides 8–19. Although our knowledge of potential serum protein biomarkers for major depression patients remains limited, some proteins have been proposed to correlate with major depression, including lipoproteins [e.g., high‐density lipoproteins (HDLs), low‐density lipoproteins (LDLs), and very‐low‐density lipoproteins (VLDLs)], α ‐enolase, glutathione S ‐transferase Yb3, BDNF, and 61 S ribosomal proteins L28 20–22.…”