Abstract
Hypotheses about the pathophysiology of depression have evolved over time. This chapter covers the most important findings in this regard. First, the classical monoamine hypothesis posited that depression is caused by an alteration in levels of one or more of the monoamines: serotonin, norepinephrine, and dopamine. More recently, research on the glutamatergic system has aroused great interest by examining the mechanism of action of ketamine, an N-methyl-D-aspartic acid (NMDA) receptor antagonist. Likewise, stressful life events can precipitate depressive episodes in vulnerable individuals. Abnormalities in the HPA axis have been associated with a hyperactive response to stress in depressed patients (the diathesis-stress model). Increased levels of inflammatory markers have been found in patients with depression and anti-inflammatory agents are being studied as antidepressants. Reduced production of BDNF and neuroplasticity can lead to depression. These pathophysiological mechanisms are reciprocally connected with each other. Major Depression is a heterogeneous entity and a variety of biological mechanisms may be involved.
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Department of Psychiatry, North Campus, Faculty of Medicine, University of Chile, Santiago, Chile
Hernán Silva
- Hernán Silva
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Department of Psychiatry and Mental Health East, Faculty of Medicine, University of Chile, Millennium Institute for Research in Depression and Personality (MIDAP), Santiago, RM, Chile
Juan Pablo Jiménez
Department of Psychiatry and Mental Health East, Faculty of Medicine, University of Chile, Millennium Institute for Research in Depression and Personality (MIDAP), Santiago, RM, Chile
Alberto Botto
Research Department of Clinical Educational and Health Psychology, University College London, London, UK
Peter Fonagy
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Silva, H. (2021). Neurobiology of Depression. In: Jiménez, J.P., Botto, A., Fonagy, P. (eds) Etiopathogenic Theories and Models in Depression. Depression and Personality. Springer, Cham. https://doi.org/10.1007/978-3-030-77329-8_8
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