Chronic Mild Stress (CMS) Revisited: Consistency and Behavioural-Neurobiological Concordance in the Effects of CMS

By P. Willner. Neuropsychobiology, 2005

1,632 citations recorded by the source corpus.

Subfields: Behavioral Neuroscience, Biological Psychiatry, Social Psychology

View Paper: https://www.semanticscholar.org/paper/56ba43aacb2f477e71101d7f6edd5693e5f9481d

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Citations in the corpus

Glutamate NMDA receptor antagonists rapidly reverse behavioral and synaptic deficits caused by chronic stress exposure (2011, neutral): “In the current study we utilized a chronic unpredictable stress (CUS) paradigm, which results in anhedonia, a core symptom of depression, that is responsive to chronic (3 weeks) but not acute or short-term antidepressant treatment (12).”
Depression, Stress, and Anhedonia: Toward a Synthesis and Integrated Model (2014, background): “This approach was subsequently modified by Willner, who developed the chronic mild stress (CMS) model, in which animals are exposed to a variety of relatively mild stressors over a prolonged period of time (Willner 2005).”
The role of neurotrophic factors in adult hippocampal neurogenesis, antidepressant treatments and animal models of depressive-like behavior (2007, background): “Despite inherent difficulties in establishing this procedure, an increasing number of studies indicate that CMS/CUS models of depressive-like behavior can be reliably and successfully performed in mice (Willner, 2005).”
Stress, Depression, and Neuroplasticity: A Convergence of Mechanisms (2008, background): “…animals, stress can lead to atrophy of the hippocampus similar to that seen in depression (Sapolsky, 2000); chronic stress paradigms in animals recapitulate many of the core behavioral characteristics of depression and are responsive to antidepressant treatment (reviewed in Willner, 2005).”
Brain-Derived Neurotrophic Factor and Neuropsychiatric Disorders (2012, background): “In rodents, chronic stress is a generally accepted model of depression because it leads to neurochemical and behavioral alterations that are analogous to those observed in depressed human patients, including increases in stress hormones, hippocampal atrophy, increased anxiety- and depression-related”