@prefix dcat: . @prefix dct: . @prefix foaf: . @prefix vcard: . @prefix xsd: . a dcat:Dataset ; dct:description """ Voltage-gated sodium channels, or Nav channels, play a key role in neuronal excitability and in the emission and propagation of action potentials. Among the different Nav isoforms, Nav1.9 is only expressed in nociceptors and shows atypical electrophysiological properties which, if they exclude a possible contribution to the depolarizing phase of the action potential, could be important for the modulation of nociceptors' excitability. This study aims to characterize the Nav1.9 implication in the pathophysiology of pain using behavioral, molecular and functional approaches. The first part of this work is to assess the Nav1.9 contribution to inflammatory pain. Therefore we have performed several behavioral tests in different inflammatory pain models (acute, subacute, chronic), using knock-out (KO) mice and rats treated with antisense oligodeoxynucleotides. Nav1.9 expression and electrophysiological properties are then analyzed within the same animal models. First, we observe that Nav1.9 channels do not contribute to pain perception in response to noxious heat or pressure in healthy animals. However, thermal and mechanical pain hypersensitivity induced by subacute (intraplantar carrageenan) or chronic (monoarthritis) inflammation is significantly lowered in Nav1.9 knock-out mice. Similar results are obtained on the subacute inflammation model using a knock-down strategy in rats. A weak reduction followed by a strong increase in Nav1.9 protein expression is observed in mice dorsal root ganglions innervating the inflamed paw during subacute inflammation. We also observe an increase in Nav1.9 immunolabeling in cutaneous nerve trunks innervating this zone. Whereas the newly produced channels do not contribute to the sodium current recorded in dorsal root ganglion cell bodies, as assessed by patch clamp, our data suggest that they are transported to nerve terminals where they could become functional and increase neuronal excitability. In the second part of this study, we aim to characterize the implication of Nav1.9 channels in cold perception and in oxaliplatin-induced cold hypersensitivity. Indeed, we surprisingly observed that Nav1.9 KO mice showed higher pain thresholds to intense cold (<10°C) than wild-type mice. This observation is confirmed by several behavioral tests in KO mice and in antisense-treated rats. As oxaliplatine (a platinum salt used to treat colorectal cancer) is known to induce cold pain hypersensitivity in most of the patients, we decided to study the Nav1.9 contribution to this symptom. Following acute oxaliplatin injection, a strong cold hypersensitivity is observed in wild-type mice at 20°C and below. We show that Nav1.9 KO results in a suppression of cold hypersensitivity to non-noxious temperatures (20 and 15°C, allodynia), and a reduction of hypersensitivity to noxious cold (10 and 5°C, hyperalgesia). A similar observation is made using Nav1.9 knock-down in rats. To conclude, our data shows that Nav1.9 could be potentially a good target to treat acute to chronic inflammatory pain, as well as oxaliplatin-induced cold hypersensitivity. Furthermore, as Nav1.9 is not involved in defining pain thresholds of healthy animals (except for noxious cold), its blockade would have anti-hyperalgesic rather than analgesic effects, which is conceptually interesting. """ ; dct:identifier "NNT: 2011CLF1MM28" ; dct:issued "2026-05-09T23:30:13.171356"^^xsd:dateTime ; dct:language "fr" ; dct:modified "2026-05-09T23:30:13.171360"^^xsd:dateTime ; dct:publisher ; dct:title "Role of Nav1.9 sodium channel in inflammatory pain, perception of cold, and oxaliplatin-induced hypersensitivity to cold." ; dcat:contactPoint [ a vcard:Organization ; vcard:fn "CCSD" ] ; dcat:distribution ; dcat:keyword "allodynia", "allodynie", "canaux-sodique", "douleur", "inflammation", "infoeu-reposemanticsdoctoralthesis", "ion-channel", "mouse", "nav19", "neuropathie", "nocicepteur", "nociceptor", "pain", "rat", "scn11a", "sdvmheplife-sciences-q-biohuman-health-and-pathology", "souris", "theses", "voltage-gated-sodium-channel" ; dcat:landingPage . a dcat:Distribution ; dct:format "HTML" ; dct:issued "2026-05-09T23:30:13.186591"^^xsd:dateTime ; dct:modified "2026-05-09T23:30:13.153711"^^xsd:dateTime ; dct:title "Role of Nav1.9 sodium channel in inflammatory pain, perception of cold, and oxaliplatin-induced hypersensitivity to cold." ; dcat:accessURL . a foaf:Agent ; foaf:name "test_moissonnage_selune" . a foaf:Document .