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[The role of the glutamatergic system in pathophysiology and pharmacotherapy for depression: preclinical and clinical data].

Georgios Paslakis, P Gass, Michael Deuschle

Fortschritte der Neurologie · Psychiatrie April 2011 DOI: 10.1055/s-0029-1245770 (opens in new tab)

Study at a glance

AI-extracted from the abstract
Characteristics Review Peer reviewed
Topics Depression
Key findings Argues that glutamatergic system dysfunction, possibly due to glial cell loss, may contribute to depression, and that antiglutamatergic agents and NMDA-receptor antagonists show promise as antidepressants, though evidence is mostly preclinical.

Abstract

An increasing significance has been attributed to the glutamatergic system in the pathophysiology of affective disorders. Glutamate is the most important excitatory neurotransmitter in the central nervous system. Glia cells are crucial regulators of the glutamatergic metabolism. Several studies have reported a dysfunction or reduced number of glia cells in patients suffering from depression. This could result in hyperfunctioning of the glutamatergic system leading to a toxic accumulation of glutamate. Commonly used antidepressants influence the glutamate metabolism and antiglutamatergic substances [e. g., riluzol] and NMDA-receptor antagonists [e. g., ketamine] have shown antidepressant properties in mostly preclinical and some clinical trials. Further substances are currently being investigated. This review provides an insight into the newest developments in this field.

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