ArticleFrontiers in neuroscience2020
Neuronal CXCL10/CXCR3 Axis Mediates the Induction of Cerebral Hyperexcitability by Peripheral Viral Challenge.
Article in Frontiers in neuroscience, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 36 citations in OpenAlex.
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- A 3D Human Neuron-on-Chip Platform to Monitor Neuronal Injury Responses.Advanced healthcare materials · 2026Article
- TNF-α induces type I IFN signalling to suppress neurogenesis and recruit T cells.Nature communications · 2026Article
- From insult to hyperexcitability: pharmacological targeting of MyD88 and JAK/STAT3 pathways in epilepsy.Inflammopharmacology · 2026Review
- CXCL10 Involvement in Vestibular Migraine via the PI3K/AKT Signaling Pathway.CNS neuroscience & therapeutics · 2025Article
- C‑X‑C Motif Chemokine 10/C-X‑C Motif Chemokine Receptor 3 Signaling Induces Neural Senescence and Cognitive Impairments.ACS pharmacology & translational science · 2025Article
- Astrocyte-derived CXCL10 exacerbates endothelial cells pyroptosis and blood-brain barrier disruption via CXCR3/cGAS/AIM2 pathway after intracerebral hemorrhage.Cell death discovery · 2025Article
- Human Brain Organoids: A New Model to StudyJournal of fungi (Basel, Switzerland) · 2025Article
- EphB2-mediated ephrin-B reverse signaling on microglia drives an anti-viral, but inflammatory and neurotoxic response associated with HIV.Journal of neuroinflammation · 2025Article
- CCL21-CCR7 blockade prevents neuroinflammation and degeneration in Parkinson's disease models.Journal of neuroinflammation · 2025Article
- Differential immunometabolic responses to Delta and Omicron SARS-CoV-2 variants in golden syrian hamsters.iScience · 2024Article
- SARS-CoV-2-Induced Type I Interferon Signaling Dysregulation in Olfactory Networks Implications for Alzheimer's Disease.Current issues in molecular biology · 2024Article
- CXCL10 is a crucial chemoattractant for efficient intranasal delivery of mesenchymal stem cells to the neonatal hypoxic-ischemic brain.Stem cell research & therapy · 2024Article
- A pre-existing Toxoplasma gondii infection exacerbates the pathophysiological response and extent of brain damage after traumatic brain injury in mice.Journal of neuroinflammation · 2024Article
- Type I interferon signaling, cognition and neurodegeneration following COVID-19: update on a mechanistic pathogenetic model with implications for Alzheimer's disease.Frontiers in human neuroscience · 2024Article
- Peripheral viral challenge increases c-fos level in cerebral neurons.Metabolic brain disease · 2021Article
- Article
- Paeonol Ameliorates Chronic Itch and Spinal Astrocytic Activation via CXCR3 in an Experimental Dry Skin Model in Mice.Frontiers in pharmacology · 2021Article
- Article
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Authors and funding
11 authors at 3 institutions in 2 countries.
Funding
Abstract
Peripheral infections can potently exacerbate neuropathological conditions, though the underlying mechanisms are poorly understood. We have previously demonstrated that intraperitoneal (i.p.) injection of a viral mimetic, polyinosinic-polycytidylic acid (PIC) induces a robust generation of CXCL10 chemokine in the hippocampus. The hippocampus also features hyperexcitability of neuronal circuits following PIC challenge. The present study was undertaken to determine the role of CXCL10 in mediating the development of hyperexcitability in response to PIC challenge. Briefly, young female C57BL/6 mice were i.p. injected with PIC, and after 24 h, the brains were analyzed by confocal microscopy. CXCL10 staining of neuronal perikarya and a less intense staining of the neuropil was observed in the hippocampus and cortex. CXCL10 staining was also evident in a subpopulation of astrocytes, whereas microglia were CXCL10 negative. CXCR3, the cognate receptor of CXCL10 was present exclusively on neurons, indicating that the CXCL10/CXCR3 axis operates through an autocrine/paracrine neuronal signaling. Blocking cerebral CXCR3 through intracerebroventricular injection of a specific inhibitor, AMG487, abrogated PIC challenge-induced increase in basal synaptic transmission and long-term potentiation (LTP), as well as the reduction of paired-pulse facilitation (PPF), in the hippocampus. The PIC-mediated abolishment of hippocampal long-term depression (LTD) was also restored after administration of AMG487. Moreover, CXCR3 inhibition attenuated seizure hypersensitivity induced by PIC challenge. The efficacy of AMG487 strongly strengthens the notion that CXCL10/CXCR3 axis mediates the induction of cerebral hyperexcitability by PIC challenge.
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