Abstract
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.
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