ArticleJournal of pain research2017
Neuronal plasticity of trigeminal ganglia in mice following nerve injury.
Article in Journal of pain research, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed.
- Perioperative changes in inflammatory biomarkers and underlying molecular mechanisms in patients with trigeminal neuralgia undergoing surgical interventions.Frontiers in neurology · 2025Review
- The CSF1-CSF1R pathway in the trigeminal ganglion mediates trigeminal neuralgia via inflammatory responses in mice.Molecular biology reports · 2024Article
- Lipopolysaccharide-induced Trigeminal Ganglion Nerve Fiber Damage is Associated with Autophagy Inhibition.Current medical science · 2023Article
- Trigeminal ganglion itself can be a viable target to manage trigeminal neuralgia.The journal of headache and pain · 2022Review
- A multi-staged neuropeptide response to traumatic brain injury.European journal of trauma and emergency surgery : official publication of the European Trauma Society · 2022Article
- Potential Molecular Targets for Treating Neuropathic Orofacial Pain Based on Current Findings in Animal Models.International journal of molecular sciences · 2021Review
- Expression and regulation of FRMD6 in mouse DRG neurons and spinal cord after nerve injury.Scientific reports · 2020Article
- Article
- Antagonism of Transient Receptor Potential Ankyrin Type-1 Channels as a Potential Target for the Treatment of Trigeminal Neuropathic Pain: Study in an Animal Model.International journal of molecular sciences · 2018Article
- Animal models - Mimicking the pain of trigeminal neuralgia.Indian journal of pharmacologyReview
- Histone deacetylase inhibitors prevent persistent hypersensitivity in an orofacial neuropathic pain model.Molecular painArticle
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7 authors.
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Abstract
backgroundNerve injury may induce neuropathic pain. In studying the mechanisms of orofacial neuropathic pain, attention has been paid to the plastic changes that occur in the trigeminal ganglia (TGs) and nucleus in response to an injury of the trigeminal nerve branches. Previous studies have explored the impact of sciatic nerve injury on dorsal root ganglia (DRGs) and it has shown dramatic changes in the expression of multiple biomarkers. In large, the changes in biomarker expression in TGs after trigeminal nerve injury are similar to that in DRGs after sciatic nerve injury. However, important differences exist. Therefore, there is a need to study the plasticity of biomarkers in TGs after nerve injury in the context of the development of neuropathic pain-like behaviors.
aimThe aim of this study was to investigate the plasticity of biomarkers associated with chronic persistent pain in TGs after trigeminal nerve injury. MATERIALS AND
methodsTo mimic the chronic nature of the disorder, we used an intraoral procedure to access the infraorbital nerve (ION) and induced a nerve injury in mice. Immunohistochemistry and quantification were used for revealing the expression level of each biomarker in TGs after nerve injury.
resultsTwo weeks after partial ION injury, immunohistochemistry results showed strongly upregulated expressions of activating transcription factor 3 and neuropeptide Y (NPY) in the ipsilateral TGs. Microglial cells were also activated after nerve injury. In regard to positive neuronal profile counting, however, no significant difference in expression was observed in galanin, substance P, calcitonin gene-related peptide, neuronal nitric oxide synthase, phosphorylated AKT, or P2X3 in ipsilateral TGs when compared to contralateral TGs.
conclusionIn this study, the expression and regulation of biomarkers in TGs have been observed in response to trigeminal nerve injury. Our results suggest that NPY and Iba1 might play crucial roles in the pathogenesis of orofacial neuropathic pain following this type of injury. Further investigations on the relevance of these changes may help to target suitable treatment possibilities for trigeminal neuralgia.
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