Pain behavior in SCN9A (Nav1.7) and SCN10A (Nav1.8) mutant rodent models
| العنوان: | Pain behavior in SCN9A (Nav1.7) and SCN10A (Nav1.8) mutant rodent models |
|---|---|
| المؤلفون: | Celeste Chidiac, Yann Herault, Yaping Xue, Claire Gaveriaux-Ruff |
| المساهمون: | Institut de Génétique et de Biologie Moléculaire et Cellulaire (IGBMC), Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)-Université de Strasbourg (UNISTRA), Herault, Yann, Université de Strasbourg (UNISTRA)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS) |
| المصدر: | Neuroscience Letters Neuroscience Letters, Elsevier, 2021, 753, pp.135844. ⟨10.1016/j.neulet.2021.135844⟩ Neuroscience Letters, 2021, 753, pp.135844. ⟨10.1016/j.neulet.2021.135844⟩ |
| سنة النشر: | 2021 |
| مصطلحات موضوعية: | 0301 basic medicine, SCN10A, Nociception, [SDV.GEN] Life Sciences [q-bio]/Genetics, medicine.disease_cause, Bioinformatics, Neuropathic pain, Mice, 0302 clinical medicine, Loss of Function Mutation, Medicine, Nav1.7, ComputingMilieux_MISCELLANEOUS, Nav1.8, Mice, Knockout, Voltage-Gated Sodium Channel Blockers, Mutation, Analgesics, SCN9A, General Neuroscience, NAV1.7 Voltage-Gated Sodium Channel, medicine.anatomical_structure, Peripheral nervous system, Gain of Function Mutation, Rats, Transgenic, Life Sciences & Biomedicine, Rodent model, Knockout, Small Fiber Neuropathy, Analgesic, Pain, NAV1.8 Voltage-Gated Sodium Channel, 03 medical and health sciences, Noxious stimulus, Animals, Humans, [SDV.GEN]Life Sciences [q-bio]/Genetics, Science & Technology, Mechanism (biology), business.industry, Sodium channel, [SCCO.NEUR]Cognitive science/Neuroscience, [SCCO.NEUR] Cognitive science/Neuroscience, Neurosciences, Mutant, Pain behavior, Voltage-Gated Sodium Channel Agonists, Rats, Disease Models, Animal, 030104 developmental biology, NAV1, Neurosciences & Neurology, business, 030217 neurology & neurosurgery |
| الوصف: | The two voltage gated sodium channels Nav1.7 and Nav1.8 are expressed in the peripheral nervous system and involved in various pain conditions including inflammatory and neuropathic pain. Rodent models bearing deletions or mutations of the corresponding genes, Scn9a and Scn10a, were created in order to understand the role of these channels in the pathophysiological mechanism underlying pain symptoms. This review summarizes the pain behavior profiles reported in Scn9a and Scn10a rodent models. The complete loss-of-function or knockout (KO) of Scn9a or Scn10a and the conditional KO (cKO) of Scn9a in specific cell populations were shown to decrease sensitivity to various pain stimuli. The Possum mutant mice bearing a dominant hypermorphic mutation in Scn10a revealed higher sensitivity to noxious stimuli. Several gain-of-function mutations were identified in patients with painful small fiber neuropathy. Future knowledge obtained from preclinical models bearing these mutations will allow understanding how these mutations affect pain. In addition, the review gives perspectives for creating models that better mimic patients' pain symptoms in view to developing novel analgesic strategies. ispartof: NEUROSCIENCE LETTERS vol:753 ispartof: location:Ireland status: published |
| وصف الملف: | Print-Electronic |
| تدمد: | 0304-3940 |
| DOI: | 10.1016/j.neulet.2021.135844 |
| DOI: | 10.1016/j.neulet.2021.135844⟩ |
| URL الوصول: | https://explore.openaire.eu/search/publication?articleId=doi_dedup___::4cc5c7eba558762368899209c8f880d3 |
| Rights: | OPEN |
| رقم الانضمام: | edsair.doi.dedup.....4cc5c7eba558762368899209c8f880d3 |
| قاعدة البيانات: | OpenAIRE |
| تدمد: | 03043940 |
|---|---|
| DOI: | 10.1016/j.neulet.2021.135844 |