Objective:Biological markers of the ventrolateral orbitofrontal cortex(vlOFC)involved in pain regula-tion were screened.Methods:Chronic inflammatory pain was induced in male C57BL/6J mice by injection of complete Freund's adjuvant(CFA)into the left posterior plantar.Paw withdrawal threshold(PWT)and paw withdrawal latency(PWL)were detected to evalue hyperalgesia.Transcriptome sequencing was performed on fresh tissue from vlOFC of mice after behavioral tests.The differentially expressed genes(DEGs)were screened by bioinformatics method,and their biological functions and pathways were enriched.Results:Compared with the PBS group,the left hindpaw me-chanical pain threshold and the paw withdrawal latency caused by heat pain were significantly reduced in the CFA group(P＜0.001).The DEGs of vlOFC in the two groups were 497,of which 143 were up-regulated and 354 were down-reg-ulated.Gene Ontology(GO)and Kyoto Encyclopedia of Genes and Genomes(KEGGs)analysis showed that:In chro-nic inflammatory pain model mice,DEGs of vlOFC were mainly manifested in biological processes such as organic cation transport,neurotransmitter transport,and regulation of cytoplasmic calcium ion concentration.It is related to G protein-coupled receptors(GPCRs),neuropeptides and ammonium transport.DEGs mainly focuses on neuroactive ligand-receptor interactions,cytokine-cytokine receptor interactions,and cAMP signaling pathways.Reactome functional en-richment analysis showed that the pathway with the highest number of DEGs enriched and the lowest P value-adjusted was GPCRs ligand binding.Conclusion:Ion transport,neurotransmitter transport and binding,and GPCRs-related ac-tivities in vlOFC are involved in the regulation of chronic inflammatory pain.
维普
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