<HashMap><database>biostudies-literature</database><scores/><additional><omics_type>Unknown</omics_type><volume>134(3)</volume><submitter>Wang C</submitter><pubmed_abstract>&lt;h4>Background&lt;/h4>Chronic neuropathic pain generally has a poor response to treatment with conventional drugs. Sympathectomy can alleviate neuropathic pain in some patients, suggesting that abnormal sympathetic-somatosensory signaling interactions might underlie some forms of neuropathic pain. The molecular mechanisms underlying sympathetic-somatosensory interactions in neuropathic pain remain obscure.&lt;h4>Methods&lt;/h4>Lumbar sympathectomy was performed in spared nerve injury (SNI) mice or rats, and the up-down method was used to measure the mechanical paw withdrawal threshold. Dorsal root ganglia (DRG) injection and perfusion were used to deliver virus or drugs. Methylated RNA immunoprecipitation sequencing, RNA-sequencing, and immunoelectron microscopy were used to identify neurotransmitt</pubmed_abstract><journal>British journal of anaesthesia</journal><pagination>804-816</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC11867076</full_dataset_link><repository>biostudies-literature</repository><pubmed_title>Sprouting sympathetic fibres release CXCL16 and norepinephrine to synergistically mediate sensory neuronal hyperexcitability in a rodent model of neuropathic pain.</pubmed_title><pmcid>PMC11867076</pmcid><pubmed_authors>Li C</pubmed_authors><pubmed_authors>Liu M</pubmed_authors><pubmed_authors>Wang C</pubmed_authors><pubmed_authors>Di A</pubmed_authors><pubmed_authors>Feng X</pubmed_authors><pubmed_authors>Liang Z</pubmed_authors><pubmed_authors>Wei M</pubmed_authors><pubmed_authors>Fan H</pubmed_authors><pubmed_authors>Xu T</pubmed_authors><pubmed_authors>Xin W</pubmed_authors><pubmed_authors>Wu Y</pubmed_authors><pubmed_authors>Liu F</pubmed_authors><pubmed_authors>Dong B</pubmed_authors></additional><is_claimable>false</is_claimable><name>Sprouting sympathetic fibres release CXCL16 and norepinephrine to synergistically mediate sensory neuronal hyperexcitability in a rodent model of neuropathic pain.</name><description>&lt;h4>Background&lt;/h4>Chronic neuropathic pain generally has a poor response to treatment with conventional drugs. Sympathectomy can alleviate neuropathic pain in some patients, suggesting that abnormal sympathetic-somatosensory signaling interactions might underlie some forms of neuropathic pain. The molecular mechanisms underlying sympathetic-somatosensory interactions in neuropathic pain remain obscure.&lt;h4>Methods&lt;/h4>Lumbar sympathectomy was performed in spared nerve injury (SNI) mice or rats, and the up-down method was used to measure the mechanical paw withdrawal threshold. Dorsal root ganglia (DRG) injection and perfusion were used to deliver virus or drugs. Methylated RNA immunoprecipitation sequencing, RNA-sequencing, and immunoelectron microscopy were used to identify neurotransmitt</description><dates><release>2025-01-01T00:00:00Z</release><publication>2025 Mar</publication><modification>2025-04-22T18:52:11.685Z</modification><creation>2025-04-06T02:39:10.896Z</creation></dates><accession>S-EPMC11867076</accession><cross_references><pubmed>39848871</pubmed><doi>10.1016/j.bja.2024.10.019</doi></cross_references></HashMap>