ArticleMolecular psychiatry2024
Enhanced fear memory after social defeat in mice is dependent on interleukin-1 receptor signaling in glutamatergic neurons.
Article in Molecular psychiatry, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers, 1 of them a synthesis that pooled it.
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Who cites it
20 citing papers in PubMed, 1 synthesis or guideline pooled it, 18 citations in OpenAlex.
- Inflammation as a mediating pathway between social defeat and mental health in humans: A systematic review.Translational psychiatry · 2026Pooled it
- Review
- Non-classical NMDAR subunit GluN3A in a specialized hippocampal region regulates stress-coping strategies in male mice.Communications biology · 2026Article
- Redox Regulation of the NLRP3 Inflammasome and its Implications for Immunization-related Neuroinflammation.Molecular neurobiology · 2026Review
- Orchestrating neuroinflammation: A symphony of Interleukin-1 and cell type-specific Interleukin-1 receptor type 1 signaling in the brain.Brain behavior and immunity integrative · 2026Article
- Dual roles of basal NLRP3 expression in cognitive and neurogenic aging.Biogerontology · 2026Article
- Effects of GPR110 expression on neurobehavioral outcomes in mice.Frontiers in neuroscience · 2026Article
- Sustained hippocampal neuroinflammation and subsequent glutamatergic dysfunction in juvenile idiopathic arthritis: evidence from proton magnetic resonance spectroscopy (Arthritis research & therapy · 2025Article
- Neurotransmitter signaling in molecular and behavioral immune responses to pathogens inMicrobiology and molecular biology reviews : MMBR · 2025Review
- Article
- Review
- Inflammatory and Oxidative Biological Profiles in Mental Disorders: Perspectives on Diagnostics and Personalized Therapy.International journal of molecular sciences · 2025Review
- Persistent pain signaling and stress response in a mouse model of inflammatory low back pain.Pain reports · 2025Article
- Stress Sensitization of Neurons in the Dentate Gyrus Is Dependent on Neuronal Interleukin-1 Receptor Signaling and Is Associated with Increased Synaptic Plasticity, Perineuronal Nets, and Excitatory/Inhibitory Input Imbalance.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2025Article
- Diffuse traumatic brain injury induced stimulator of interferons (STING) signaling in microglia drives cortical neuroinflammation, neuronal dysfunction, and impaired cognition.Journal of neuroinflammation · 2025Article
- Diffuse Traumatic Brain Injury Induced Stimulator of Interferons (STING) Signaling in Microglia Drives Cortical Neuroinflammation, Neuronal Dysfunction, and Impaired Cognition.Research square · 2025Article
- A Clinically Aligned Murine Model of Electroconvulsive Stimulation Reverses Social Aversion and Displays Fear Memory Impairment After Chronic Social Defeat Stress.bioRxiv : the preprint server for biology · 2025Article
- Repeated social defeat in male mice induced unique RNA profiles in projection neurons from the amygdala to the hippocampus.Brain, behavior, & immunity - health · 2025Article
- Localization of brain neuronal IL-1R1 reveals specific neural circuitries responsive to immune signaling.Journal of neuroinflammation · 2024Article
- Novel microglial transcriptional signatures promote social and cognitive deficits following repeated social defeat.Communications biology · 2024Article
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 1 country.
Funding
Abstract
Chronic stress is associated with increased anxiety, cognitive deficits, and post-traumatic stress disorder. Repeated social defeat (RSD) in mice causes long-term stress-sensitization associated with increased microglia activation, monocyte accumulation, and enhanced interleukin (IL)-1 signaling in endothelia and neurons. With stress-sensitization, mice have amplified neuronal, immune, and behavioral responses to acute stress 24 days later. This is clinically relevant as it shares key aspects with post-traumatic stress disorder. The mechanisms underlying stress-sensitization are unclear, but enhanced fear memory may be critical. The purpose of this study was to determine the influence of microglia and IL-1R1 signaling in neurons in the development of sensitization and increased fear memory after RSD. Here, RSD accelerated fear acquisition, delayed fear extinction, and increased cued-based freezing at 0.5 day. The enhancement in contextual fear memory after RSD persisted 24 days later. Next, microglia were depleted with a CSF1R antagonist prior to RSD and several parameters were assessed. Microglia depletion blocked monocyte recruitment to the brain. Nonetheless, neuronal reactivity (pCREB) and IL-1β RNA expression in the hippocampus and enhanced fear memory after RSD were microglial-independent. Because IL-1β RNA was prominent in the hippocampus after RSD even with microglia depletion, IL-1R1 mediated signaling in glutamatergic neurons was assessed using neuronal Vglut2
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.