ArticleFrontiers in pharmacology2018
Blocking p38 Signaling Reduces the Activation of Pro-inflammatory Cytokines and the Phosphorylation of p38 in the Habenula and Reverses Depressive-Like Behaviors Induced by Neuroinflammation.
Article in Frontiers in pharmacology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed, 50 citations in OpenAlex.
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- Paroxetine Triggers Inflammatory State on Zebrafish Early Embryonic Development.Life (Basel, Switzerland) · 2025Article
- Herpesvirus initiation of dementias and autoimmune diseases.Journal of neurovirology · 2025Review
- Pentoxifylline Prevents Neuroinflammation and Modifies PTEN/TrkB Signaling in an LPS-Induced Depression Model.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2025Article
- The Antidepressant- and Anxiolytic-Like Effects of the Phosphodiesterase Type-5 Inhibitor Tadalafil are Associated with the Modulation of the Gut-Brain Axis During CNS Autoimmunity.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2024Article
- eIF4E phosphorylation mediated LPS induced depressive-like behaviors via ameliorated neuroinflammation and dendritic loss.Translational psychiatry · 2023Article
- Immunostimulatory activity of fluoxetine in macrophages via regulation of the PI3K and P38 signaling pathways.Immunologic research · 2023Article
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- Chemical Knockdown of Phosphorylated p38 Mitogen-Activated Protein Kinase (MAPK) as a Novel Approach for the Treatment of Alzheimer's Disease.ACS central science · 2023Article
- Yomogin, Isolated fromAntioxidants (Basel, Switzerland) · 2022Article
- History and main research of psychoneuroimmunology in China.Brain, behavior, & immunity - health · 2022Article
- Pinocembrin Inhibits P2X4 Receptor-Mediated Pyroptosis in Hippocampus to Alleviate the Behaviours of Chronic Pain and Depression Comorbidity in Rats.Molecular neurobiology · 2022Article
- Article
- The Role of the Lateral Habenula in Suicide: A Call for Further Exploration.Frontiers in behavioral neuroscience · 2022Review
- Oncogenic pathways activated by pro-inflammatory cytokines promote mutant p53 stability: clue for novel anticancer therapies.Cellular and molecular life sciences : CMLS · 2021Review
- The anti-inflammatory role of SSRI and SNRI in the treatment of depression: a review of human and rodent research studies.Inflammopharmacology · 2021Review
- Fluoxetine regulates eEF2 activity (phosphorylation) via HDAC1 inhibitory mechanism in an LPS-induced mouse model of depression.Journal of neuroinflammation · 2021Article
- Terpenoids fromInternational journal of molecular sciences · 2021Article
- Xinkeshu Improves Endothelial Function and Augments Reendothelialization Capacity in Coronary Artery Disease with Anxiety/Depression.Oxidative medicine and cellular longevity · 2021Article
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Increasing evidence has demonstrated that neuroinflammation contributes to the development of depressive-like behaviors, in both animal models and human patients; however, the brain areas and signaling pathways involved are still elusive. Recent studies have suggested novel roles of the habenula in the onset of depression and other psychiatric disorders; however, there is no evidence for whether the habenula has a function in neuroinflammation-induced depression. Using an animal model of depression, which is induced by the repeated central administration of lipopolysaccharide (LPS), we examined whether cytokine expression and p38 signal activation in the habenula were involved in the depressive-like behaviors. Body weight, saccharin preference test, and tail suspension test were used to measure depressive-like behaviors. Immunohistochemistry, quantitative-polymerase chain reaction (q-PCR), and western blot were used to measure the expression of tumor necrosis factor-α (TNF-α), interleukin-10 (IL-10), and the phosphorylation of p38 in the habenula. The results showed that central LPS administration induced depressive-like behaviors, characterized by anhedonia in the saccharin preference test and increased immobility in the tail suspension test. Central LPS administration also significantly increased the p-p38 level in microglial cells and increased TNF-α expression in the habenula. Treatment with fluoxetine, a widely prescribed antidepressant, or SB203580, a p38-specific inhibitor, reversed the depressive-like behaviors, normalized the alterations in p-p38 and TNF-α levels and increased the levels of the anti-inflammatory cytokine IL-10 in the habenula. The present findings suggest that the habenula is involved in the pathophysiology of behavioral depression induced by neuroinflammation, and the p38 pathway may serve as a novel mechanism-based target for the treatment of inflammation-related depression.
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