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Updated: Jul 11, 2026
06:55
An Unpredictable Chronic Mild Stress Protocol for Instigating Depressive Symptoms, Behavioral Changes and Negative Health Outcomes in Rodents
Published on: December 2, 2015
[Immunological aspects of depressive disorders]
1Klinik für Psychiatrie und Psychotherapie, Ludwig-Maximilians-Universität, Nussbaumstrasse 7, 80336 München. Norbert.Mueller@med.uni-muenchen.de
Der Nervenarzt
|October 12, 2007
Summary
Depression involves serotonin deficiency and excess glutamate, driven by inflammation. Immune responses activate enzymes that deplete serotonin and boost glutamate, impacting brain cell balance.
Area of Science:
- Neuroscience
- Immunology
- Psychiatry
Context:
- Depression is linked to monoamine deficiency, but increased glutamate neurotransmission is also implicated.
- The interplay between neurotransmitter dysregulation, immune activation, and morphological changes in depression requires further understanding.
Purpose:
- To present an integrated concept linking neurotransmitter imbalances, immune factors, and cellular changes in depressive disorder.
- To explore the role of proinflammatory cytokines and the enzyme indoleamine-2,3-dioxygenase (IDO) in serotonin deficiency and glutamatergic overproduction.
Summary:
- Proinflammatory cytokines increase IDO, leading to serotonin depletion and glutamate agonist production.
- IDO activation in microglial cells, coupled with decreased astrocytes, disrupts immune balance and glutamatergic neurotransmission in depression.
- This immune-astrocyte-microglia dysregulation contributes to both serotonin deficiency and glutamate overproduction.
Impact:
- Highlights the critical role of immune activation and neuroinflammation in the pathophysiology of depression.
- Suggests that targeting anti-inflammatory mechanisms, such as cyclo-oxygenase-2 (COX-2) inhibitors, may offer novel antidepressant therapeutic strategies.
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