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date: 16 June 2019

Abstract and Keywords

Neuroendocrine and neurochemical theories of depression have continued to be of importance in understanding pathophysiology and suggesting new kinds of pharmacological interventions. Monoamine theories still dominate the neurochemistry of depression and results from monoamine depletion studies suggest that in certain circumstances lowered activity of serotonin and noradrenaline pathways can indeed lead to clinical depressive symptomatology. More recent developments have implicated changes in the amino acid neurotransmitters γ-aminobutyric acid (GABA) and glutamate in depressed patients; the ability of the N-methyl-d-aspartate acid (NMDA) receptor antagonist, ketamine, to relieve depressive symptomatology rapidly has spurred basic research on the cellular mechanism of glutamatergic antidepressant action. The link between inflammation and depression has led to new kinds of immunological investigations in depressed patients and suggests the possibility of developing effective targeted antiinflammatory treatments. Finally hypothalamic–pituitary–adrenal (HPA) axis abnormalities remain a focus of interest, particularly in the context of the many medical comorbidities that frequently complicate chronic depressive disorders.

Keywords: depression, monoamine, serotonin, noradrenaline, dopamine, GABA, glutamate, ketamine, inflammation, HPA axis

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