IL-1β is an essential mediator of the antineurogenic and anhedonic effects of stress

By J. Koo, R. Duman. Proceedings of the National Academy of Sciences of the United States of America, 2008

873 citations recorded by the source corpus.

Subfields: Behavioral Neuroscience, Biological Psychiatry, Neurology

View Paper: https://www.semanticscholar.org/paper/3ff7128cb9f0d7242315f8b7a54606edbe1e49f2

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Behavioral Neuroscience

1. Andrew H. Miller
2. Charles L Raison
3. L. Capuron
4. V. Maletić
5. E. Nestler
6. E. Haroon
7. F. Lotrich
8. J. Felger

In Biological Psychiatry

1. Andrew H. Miller
2. Charles L Raison
3. V. Maletić
4. L. Capuron
5. E. Haroon
6. F. Lotrich
7. J. Felger
8. E. Nestler

In Neurology

1. Andrew H. Miller
2. Charles L Raison
3. Alok Kumar
4. E. Haroon
5. B. Leuner
6. E. Nestler
7. Michael Maes
8. Bernhard T. Baune

Citations in the corpus

• The molecular neurobiology of depression (2008, positive): “show antidepressant-like behavioural phenotypes, and a centrally administered antagonist of the IL-1β receptor reversed the behavioural and antineurogenic effects of chronic stres”
• The inflammatory & neurodegenerative (I&ND) hypothesis of depression: leads for future research and new drug developments in depression (2009, background): “In animal models of depression, rodents were found to display reduced hippocampal neurogenesis (Goshen et al. 2008; Koo and Duman 2008) along with decreases in the levels of BDNF in brain regions associated with depression (Schmidt and Duman 2007; Fuchs et al. 2004).”
• Neuroinflammation and depression: A review (2020, background): “…to IL-1β or to its inducers LPS and IFN-α decrease hippocampal neurogenesis and promote depressive-like behaviours in mice (Goshen et al., 2008; Koo & Duman, 2008) and rats (Kaneko et al., 2006; Monje et al., 2003), as found to occur after both acute in vitro injection (Green & Nolan, 2012;…”
• Inflammation in Fear- and Anxiety-Based Disorders: PTSD, GAD, and Beyond (2017, background): “Prolonged exposure to stressful stimuli that elicit fear and anxiety in PTSD, GAD, PD, and phobias activate both central and peripheral immune cells to release cytokines, such as IL-1β (Koo and Duman, 2008; Maier and Watkins, 1998).”
• BRAIN REGENERATION IN PHYSIOLOGY AND PATHOLOGY: THE IMMUNE SIGNATURE DRIVING THERAPEUTIC PLASTICITY OF NEURAL STEM CELLS (2011, background): “IL-1 promotes the decrease of proliferating cells in the SGZ when induced by acute stress or ectopically expressed within the brain (by means of a recombinant adenoviral vector) (111, 145).”
• Immune System to Brain Signaling: Neuropsychopharmacological Implications (2011, background): “…cells or the use of IL-1 knockout mice reverses the reduced growth factor production (i.e. BDNF) and decreased neurogenesis that is associated with chronic stress (while also reversing stressinduced behavioral changes) (Ben Menachem-Zidon et al., 2008; Goshen et al., 2008; Koo and Duman, 2008).”
• Psychoneuroimmunology Meets Neuropsychopharmacology: Translational Implications of the Impact of Inflammation on Behavior (2012, background): “IDO is activated by a number of cytokines alone or in combination, including IFN-g, TNF-a, IL-1, and IL-6, through stimulation of cytokine-signaling pathways such as signal transducer and activator of transcription (STAT)-1, IFN-regulatory factor-1, p38 mitogen-activated protein kinase (MAPK), and N”
• Microglia in the TBI Brain: The Good, The Bad, And The Dysregulated (2015, background): “…demonstrated that several pro-inflammatory cytokines produced by M1-like microglia and macrophages, such as IFNγ, IL-1β, TNFα, and IL-6, can also suppress neurogenesis (Ben-Hur et al., 2003; Cacci et al., 2005; Iosif et al., 2008; Koo and Duman, 2008; Monje et al., 2003; Vallieres et al., 2002).”
• Structural Plasticity and Hippocampal Function (2010, background): “…widespread acceptance that the adult brain is capable of undergoing dramatic structural reorganization, it is likely only a matter of time before definitive conclusions are obtained about the precise role of structural plasticity in hippocampal functions under normal and pathological conditions.”
• Inflammatory Cytokines in Depression: Neurobiological Mechanisms and Therapeutic Implications (2013, background): “Physical and psychological stressors can activate immune cells in both the periphery and CNS to release inflammatory cytokines that lead to neurotransmitter changes and behavioral alterations (Maier and Watkins, 1998, Koo and Duman, 2008).”
• Immune modulation of learning, memory, neural plasticity and neurogenesis. (2011, background): “Furthermore, this anti-neurogenic effect was found to be mediated by activation of NfjB signaling pathway, and could be blocked by IL-1ra (Koo and Duman, 2008).”