Chronic pain is a major health problem, which can impair quality of life and reduce productivity. Electroacupuncture (EA), a modality of medicine based on the theories of Traditional Chinese Medicine (TCM), presents great therapeutic effects on chronic pain. Its clinical application has gained increasing popularity, and in parallel, more research has been performed on the mechanisms of EA-induced analgesia. The past decades have seen enormous advances both in neuronal circuitry of needle-insertion and in its molecular mechanism. EA may block pain by activating the descending pain inhibitory system, which originates in the brainstem and terminates at the spinal cord. This review article synthesizes corresponding studies to elucidate how EA alleviate pain via the mediation of this descending system. Much emphasis has been put on the implication of descending serotonergic and noradrenergic pathways in the process of pain modulation. Also, other important transmitters and supraspinal regions related to analgesic effects of EA have been demonstrated. Finally, it should be noticed that there exist some shortcomings involved in the animal experimental designed for EA, which account for conflicting results obtained by different studies.

Glaucoma and traumatic optic nerve crush (ONC) injury result in progressive loss of retinal ganglion cells (RGCs) and defects in visual function. In clinical trials of Traditional Chinese Medicine, acupuncture has been widely used for the treatment of ocular diseases. However, the molecular mechanisms of acupuncture treatment are still unclear. In this study, we used technique of RNA sequencing (RNA-seq) to study the effects of acupuncture treatment on retinal transcriptome after axotomy injury. RNA-seq results revealed that 436 genes including 31 transcription factors (TFs) were changed after injury, among them were many well-known neural degeneration related TFs such as Jun, Ddit3, Atf3, and Atf4. Interestingly, acupuncture treatment at acupoint GB20 (Fengchi) significantly reversed a series of differential expressed genes (DEGs) induced by optic nerve injury. While treatments at BL1 (Jingming) or GB20 sham control acupoint-GV16 (Fengfu), led to limited DEG reversal. In contrast, treatments at these two sites further enhanced the trend of DEG expression induced by axotomy injury. At last, retina immunostaining results revealed that only GB20 acupoint treatment increased RGC survival, in consistent with RNA-seq results. Therefore, our study first reported that acupuncture treatment regulated retinal transcriptome and reversed the gene expression induced by axotomy injury, and GB20 acupoint treatment increased RGC survival, which will provide novel therapeutic targets for treatment of ocular diseases.

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Optic neuritis (ON) is one of the most frequent symptoms of multiple sclerosis (MS) that results in progressive loss of axons and neurons. In clinical trials of Traditional Chinese Medicine, needling at the GB20 acupoint has been widely used for the treatment of ocular diseases, including ON. However, the molecular mechanisms of needling at this site are still unclear. In this study, we generated an experimental autoimmune encephalomyelitis (EAE) mouse model and investigated the effects of needling treatment at the GB20 acupoint on retina with EAE-associated ON. RNA sequencing of the retinal transcriptome revealed that, of the 234 differentially expressed genes induced by ON, 100 genes were upregulated, and 134 genes were downregulated by ON, while needling at the GB20 acupoint specifically reversed the expression of 21 genes compared with control treatment at GV16 acupoint. Among the reversed genes, Nr4a3, Sncg, Uchl1, and Tppp3 were involved in axon development and regeneration and were downregulated by ON, indicating the beneficial effect of needling at GB20. Further gene ontology (GO) enrichment analysis revealed that needling at GB20 affected the molecular process of Circadian rhythm in mouse retina with ON. Our study first reported that needling treatment after ON at the GB20 acupoint regulated gene expression of the retina and reversed the expression of downregulated axon development-related genes. This study also demonstrated that GV16 was a perfect control treatment site for GB20 in animal research. Our study provided a scientific basis for needling treatments at GB20 for ocular diseases.