Inflammation, Glutamate, and Glia in Depression: A Literature Review

Journal Article

ABSTRACTMultiple lines of evidence suggest that inflammation and glutamate dysfunction contribute to the pathophysiology of depression. In this review we provide an overview of how these two systems may interact. Excess levels of inflammatory mediators occur in a subgroup of depressed patients. Studies of acute experimental activation of the immune system with endotoxin and of chronic activation during interferon-α treatment show that inflammation can cause depression. Peripheral inflammation leads to microglial activation which could interfere with excitatory amino acid metabolism leading to inappropriate glutamate receptor activation. Loss of astroglia, a feature of depression, upsets the balance of anti- and pro-inflammatory mediators and further impairs the removal of excitatory amino acids. Microglia activated by excess inflammation, astroglial loss, and inappropriate glutamate receptor activation ultimately disrupt the delicate balance of neuroprotective versus neurotoxic effects in the brain, potentially leading to depression.

Full Text

Duke Authors

Cited Authors

  • McNally, L; Bhagwagar, Z; Hannestad, J

Published Date

  • June 2008

Published In

Volume / Issue

  • 13 / 6

Start / End Page

  • 501 - 510

Published By

Electronic International Standard Serial Number (EISSN)

  • 2165-6509

International Standard Serial Number (ISSN)

  • 1092-8529

Digital Object Identifier (DOI)

  • 10.1017/s1092852900016734

Language

  • en