ArticlePloS one2013
TNFα levels and macrophages expression reflect an inflammatory potential of trigeminal ganglia in a mouse model of familial hemiplegic migraine.
Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.
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Who cites it
46 citing papers in PubMed, 82 citations in OpenAlex.
- Leukocyte inflammatory phenotype and function in migraine patients compared with matched non-migraine volunteers: a pilot study.BMC neurology · 2022Trial
- The synergistic effects of ω-3 fatty acids and nano-curcumin supplementation on tumor necrosis factor (TNF)-α gene expression and serum level in migraine patients.Immunogenetics · 2017Trial
- Trigeminal nerve microstructure is linked with neuroinflammation and brainstem activity in migraine.Brain : a journal of neurology · 2025Article
- Models of Trigeminal Activation: Is There an Animal Model of Migraine?Brain sciences · 2024Review
- Causal association between systemic lupus erythematosus and the risk of migraine: A Mendelian randomization study.Brain and behavior · 2024Article
- Causality between multiple autoimmune disorders and migraine and its subtypes: a two-sample Mendelian randomization study.Frontiers in neurology · 2024Article
- Role of TNFPain research & management · 2024Review
- Optogenetic cortical spreading depolarization induces headache-related behaviour and neuroinflammatory responses some prolonged in familial hemiplegic migraine type 1 mice.The journal of headache and pain · 2023Article
- Modulation of Glia Activation by TRPA1 Antagonism in Preclinical Models of Migraine.International journal of molecular sciences · 2022Article
- Review
- The role of the meningeal lymphatic system in local meningeal inflammation and trigeminal nociception.Scientific reports · 2022Article
- Changes in Plasma Lipid Levels Following Cortical Spreading Depolarization in a Transgenic Mouse Model of Familial Hemiplegic Migraine.Metabolites · 2022Article
- Involvement of TRPM2 in the Neurobiology of Experimental Migraine: Focus on Oxidative Stress and Apoptosis.Molecular neurobiology · 2021Article
- Tissue-resident M2 macrophages directly contact primary sensory neurons in the sensory ganglia after nerve injury.Journal of neuroinflammation · 2021Article
- Headache in people with epilepsy.Nature reviews. Neurology · 2021Review
- Role of Neuroinflammation and Blood-Brain Barrier Permutability on Migraine.International journal of molecular sciences · 2021Review
- Migraine and neuroinflammation: the inflammasome perspective.The journal of headache and pain · 2021Review
- Headache Medicine Grand Challenge: Headache: A New Frontier, A New Challenge.Frontiers in pain research (Lausanne, Switzerland) · 2021Article
- Chemokines and Pain in the Trigeminal System.Frontiers in pain research (Lausanne, Switzerland) · 2021Review
- Overexpressed NaFrontiers in cellular neuroscience · 2021Article
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Authors and funding
6 authors at 3 institutions in 3 countries.
Funding
Abstract
Latent changes in trigeminal ganglion structure and function resembling inflammatory conditions may predispose to acute attacks of migraine pain. Here, we investigated whether, in trigeminal sensory ganglia, cytokines such as TNFα might contribute to a local inflammatory phenotype of a transgenic knock-in (KI) mouse model of familial hemiplegic migraine type-1 (FHM-1). To this end, macrophage occurrence and cytokine expression in trigeminal ganglia were compared between wild type (WT) and R192Q mutant Ca(V)2.1 Ca(2+) channel (R192Q KI) mice, a genetic model of FHM-1. Cellular and molecular characterization was performed using a combination of confocal immunohistochemistry and cytokine assays. With respect to WT, R192Q KI trigeminal ganglia were enriched in activated macrophages as suggested by their morphology and immunoreactivity to the markers Iba1, CD11b, and ED1. R192Q KI trigeminal ganglia constitutively expressed higher mRNA levels of IL1β, IL6, IL10 and TNFα cytokines and the MCP-1 chemokine. Consistent with the report that TNFα is a major factor to sensitize trigeminal ganglia, we observed that, following an inflammatory reaction evoked by LPS injection, TNFα expression and macrophage occurrence were significantly higher in R192Q KI ganglia with respect to WT ganglia. Our data suggest that, in KI trigeminal ganglia, the complex cellular and molecular environment could support a new tissue phenotype compatible with a neuroinflammatory profile. We propose that, in FHM patients, this condition might contribute to trigeminal pain pathophysiology through release of soluble mediators, including TNFα, that may modulate the crosstalk between sensory neurons and resident glia, underlying the process of neuronal sensitisation.
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Registered trials
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