Exploring the Mechanisms of Electroacupuncture-Induced Analgesia through RNA Sequencing of the Periaqueductal Gray

• Published in: International journal of molecular sciences 2017-12, Vol.19 (1), p.2
• Main Authors: Hu, Man-Li, Zhu, Hong-Mei, Zhang, Qiu-Lin, Liu, Jing-Jing, Ding, Yi, Zhong, Ju-Ming, Vodyanoy, Vitaly, Ding, Ming-Xing
• Format: Article
• Language: English
• Subjects: Analgesia; Animals; Diazepam; Diazepam-binding inhibitor; Electroacupuncture; electroacupuncture analgesia; Encyclopedias; Gene expression; Gene Expression Profiling; Gene Ontology; Genes; Genome; Genomes; Glutamatergic transmission; Glutamic acid receptors; goat; Goats; Inhibitors; Kinases; MAP kinase; Nociception; Pain perception; Periaqueductal Gray - metabolism; Periaqueductal gray area; Prodynorphin; Proenkephalin; Proopiomelanocortin; Proprotein convertases; Proteasomes; Protein kinase; Proteins; Real-Time Polymerase Chain Reaction; Reproducibility of Results; RNA sequencing; Sequence Analysis, RNA; the periaqueductal gray; transcriptome; Ubiquitin
• ISSN: 1422-0067; 1661-6596; 1422-0067
• DOI: 10.3390/ijms19010002

Electroacupuncture (EA) can relieve various pains. However, its mechanism in terms of the transcriptome is still not well-known. To explore the full profile of EA-induced molecular modification in the central nerve system, three twins of goats were selected for a match-paired experiment: EA stimulation (60 Hz, 30 min) and none-EA (control). Goats in the EA group showed an increased ( < 0.05) nociceptive threshold compared with the control goats. Experimental goats were sacrificed at 4 h of the experiment, and the periaqueductal grays were harvested for RNA sequencing. As a result, 2651 differentially expressed genes (1803 up-regulated and 848 down-regulated genes) were found and enriched in 30 Kyoto Encyclopedia of Genes and Genomes pathways and 149 gene ontology terms. EA-regulated five neuropeptide genes ( , , , and ) were validated with quantitative PCR. Furthermore, up-regulated glutamate receptors, glutamate transporters, γ-aminobutyric acid ( ) receptors, GABA transporters, synaptotagmins or mitogen-activated protein kinase ( ) genes might contribute to EA-induced analgesia through regulating the glutamatergic synapse, GABAergic synapse, MAPKs, ribosome or ubiquitin-proteasome pathways. Our findings reveal a full profile of molecular modification in response to EA and provide a solid experimental framework for exploring the mechanisms underlying EA-induced analgesia.