ISSN 2051-8315
Psychopathology Review
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 Volume 3, Issue 1, 3-15, 2015
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Neuroendocrine and Neurochemical Processes in Depression

  Philip Cowen - University Department of Psychiatry, Warneford Hospital, Oxford, UK

Volume 3, Issue 1, 2015, Pages 3-15

Neuroendocrine and neurochemical theories of depression continued to be of importance in understanding pathophysiology and suggesting new kinds of pharmacological intervention. 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, GABA and glutamate, in depressed patients; the ability of the NMDA receptor antagonist, ketamine, rapidly to relieve depressive symptomatology has been a spur to much 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 the possibility of targeted anti-inflammatory treatments. Finally HPA axis abnormalities remain a focus of interest, particularly from the point of view of the many medical co-morbidities which frequently complicate chronic depressive disorders.

Table of Contents
Endocrine Abnormalities in Depression
 HPA Axis and Depression
 Other Neuroendocrine Mechanisms
Inflammatory Mechanisms in Depression
Neurochemical Changes in Depression
 Monoamines- 5-HT, Noradrenaline and Dopamine
  Development of methodology.
  Function of monoamines in depression.
 5-HT in Depression
 Noradrenaline and Dopamine
 Monoamine Depletion
γ-Aminobutyric Acid
Future Directions

Correspondence to
Philip Cowen, University Department of Psychiatry, Warneford Hospital, Oxford, OX3 7JX.

depression, monoamine, serotonin, noradrenaline, dopamine, tryptophan, GABA, glutamate, ketamine, inflammation, interferon, HPA axis.

Received 2 Feb 2014; Revised 24 Mar 2014; Accepted 25 Mar 2014; In Press 1 Oct 2015

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