{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Subedi A"],"funding":["NIDA NIH HHS","NIEHS NIH HHS","NINDS NIH HHS","National Institutes of Health","NIH HHS"],"pagination":["26612"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC11535536"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["14(1)"],"pubmed_abstract":["The transcription repressor REST in the dorsal root ganglion (DRG) is upregulated by peripheral nerve injury and promotes the development of chronic pain. However, the genes targeted by REST in neuropathic pain development remain unclear. The expression levels of four opioid receptor genes (Oprm1, Oprd1, Oprl1 and Oprk1) and the cannabinoid CB1 receptor (Cnr1) gene in the DRG regulate nociception. In this study, we determined the role of REST in controlling their expression in the DRG induced by spared nerve injury (SNI). SNI induced chronic pain hypersensitivity in wild-type mice and was accompanied by increased levels of Rest transcript and protein. Transcriptomic analyses of wild-type mouse DRGs suggested that SNI upregulates the expression of Rest transcripts and downregulates the tran"],"journal":["Scientific reports"],"pubmed_title":["Nerve injury inhibits Oprd1 and Cnr1 transcription through REST in primary sensory neurons."],"pmcid":["PMC11535536"],"funding_grant_id":["R33 DA049334","R01 DA041711","R01NS112280 and R61DA049334","R01 NS112280","P30 ES030285","R61 DA049334"],"pubmed_authors":["Sirito M","Grimm SL","Coarfa C","Lu Y","Ghosh K","Pan HL","Chatterjee B","McLeod SM","Etemad A","Gonzalez D","Huang Y","Ruiz E","Subedi A","Tiwari A","Majumder S","Singh SK"],"additional_accession":[]},"is_claimable":false,"name":"Nerve injury inhibits Oprd1 and Cnr1 transcription through REST in primary sensory neurons.","description":"The transcription repressor REST in the dorsal root ganglion (DRG) is upregulated by peripheral nerve injury and promotes the development of chronic pain. However, the genes targeted by REST in neuropathic pain development remain unclear. The expression levels of four opioid receptor genes (Oprm1, Oprd1, Oprl1 and Oprk1) and the cannabinoid CB1 receptor (Cnr1) gene in the DRG regulate nociception. In this study, we determined the role of REST in controlling their expression in the DRG induced by spared nerve injury (SNI). SNI induced chronic pain hypersensitivity in wild-type mice and was accompanied by increased levels of Rest transcript and protein. Transcriptomic analyses of wild-type mouse DRGs suggested that SNI upregulates the expression of Rest transcripts and downregulates the tran","dates":{"release":"2024-01-01T00:00:00Z","publication":"2024 Nov","modification":"2026-07-16T18:41:52.837Z","creation":"2025-04-04T01:20:53.785Z"},"accession":"S-EPMC11535536","cross_references":{"pubmed":["39496614"],"doi":["10.1038/s41598-024-74487-1"]}}