{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Iseppon F"],"funding":["Cancer Research UK","Versus Arthritis","NIHR Cambridge Biomedical Research Centre","Medical Research Council","UK Research and Innovation Medical Research Council","Wellcome Trust"],"pagination":["100168"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC11570969"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["16"],"pubmed_abstract":["Genetic deletion and pharmacological inhibition are distinct approaches to unravelling pain mechanisms, identifying targets and developing new analgesics. Both approaches have been applied to the voltage-gated sodium channels Na<sub>v</sub>1.7 and Na<sub>v</sub>1.8. Genetic deletion of Na<sub>v</sub>1.8 in mice leads to a loss of pain and antagonists are effective analgesics. The situation with Nav1.7 is more complex. Complete embryonic loss of Na<sub>v</sub>1.7 in humans or in mouse sensory neurons leads to anosmia as well as profound analgesia as a result of diminished neurotransmitter release. This is mediated by enhanced endogenous opioid signaling in humans and mice. In contrast, anosmia is opioid-independent. Sensory neuron excitability and autonomic function appear to be normal. Adu"],"journal":["Neurobiology of pain (Cambridge, Mass.)"],"pubmed_title":["Sodium channels Na&lt;sub&gt;v&lt;/sub&gt;1.7, Na&lt;sub&gt;v&lt;/sub&gt;1.8 and pain; two distinct mechanisms for Na&lt;sub&gt;v&lt;/sub&gt;1.7 null analgesia."],"pmcid":["PMC11570969"],"funding_grant_id":["21950","221521/Z/20/Z","185341","571476","MR/V012509/1"],"pubmed_authors":["Kanellopoulos AH","Wood JN","Woods CG","Caan G","Thalassinos K","Cubuk C","Lewis MJ","Cox JJ","Chiozzi R","Tian N","Iseppon F","Zhao J","Zhou J"],"additional_accession":[]},"is_claimable":false,"name":"Sodium channels Na&lt;sub&gt;v&lt;/sub&gt;1.7, Na&lt;sub&gt;v&lt;/sub&gt;1.8 and pain; two distinct mechanisms for Na&lt;sub&gt;v&lt;/sub&gt;1.7 null analgesia.","description":"Genetic deletion and pharmacological inhibition are distinct approaches to unravelling pain mechanisms, identifying targets and developing new analgesics. Both approaches have been applied to the voltage-gated sodium channels Na<sub>v</sub>1.7 and Na<sub>v</sub>1.8. Genetic deletion of Na<sub>v</sub>1.8 in mice leads to a loss of pain and antagonists are effective analgesics. The situation with Nav1.7 is more complex. Complete embryonic loss of Na<sub>v</sub>1.7 in humans or in mouse sensory neurons leads to anosmia as well as profound analgesia as a result of diminished neurotransmitter release. This is mediated by enhanced endogenous opioid signaling in humans and mice. In contrast, anosmia is opioid-independent. Sensory neuron excitability and autonomic function appear to be normal. Adu","dates":{"release":"2024-01-01T00:00:00Z","publication":"2024 Jul-Dec","modification":"2026-05-26T20:11:34.978Z","creation":"2025-04-21T21:43:10.034Z"},"accession":"S-EPMC11570969","cross_references":{"pubmed":["39559752"],"doi":["10.1016/j.ynpai.2024.100168"]}}