ZHAO Min,LI Han,WENG Zhijun, ZHANG Fang, LYU Tingting, WANG Shiyuan, WU Huangan Wu, LIU Hui-rong

(Shanghai Institute of Acupuncture-Moxibustion and Meridian, Shanghai 200030)

Abstract: Gastrointestinal (GI) pain is a common clinical problem, for which effective therapy is quite limited.GI pain are regulated largely by neurons in the dorsal root ganglia (DRG), and to a smaller degree by vagal afferents originating from neurons in the nodose/jugular ganglia.Those continual  stimulates  that  evoke  gastrointestinal  visceral  hypersensitivity,  can  be  mechanical 、chemical and various inflammatory mediators. In the rodent models of GI pain, DRG neurons become  hyperexcitable,  and  can  serve  as  a  source  for  chronic  pain.  Meanwhile,  inflammatory cytokines released by immune cells mediate the peripheral and central sensitization processes，for example, systemic inflammation can activate glial cells excessively, which persists even after hyperalgesia, and glial cells can also release inflammatory cytokines such as TNF-α,IL-1β.It is obvious that glia cells are another element in the pain signaling pathway, not only have they been considered as a supportive role for neurons, but also maintain the pain signal transmission together with neurons. As the main type of glial cells in sensory ganglia, satellite glial cells (SGCs) might also contribute to chronic pain in the animal pain model. Previous studies have mainly focused on the role of glial cells played in somatic pain, but less in gastrointestinal pain.  There is evidence that spinal glial cells,  primarily microglia and astrocytes, undergo hyperactivity in various pain models and contribute to the occurrence and maintenance of pain.  Besides, gap junctions also involved in the interaction between SGCs and neurons. SGCs in these ganglia were activated, and displayed  augmented  coupling  and  greater  sensitivity  to  the  pain  mediator  ATP.  This  article reviews the important role of glial cells located in the enteric nervous system, primarily sensory ganglia, spinal cord and brain in the transmission and integration of gastrointestinal pain signals.

Key words:  Neurobiology;  satellite glial cells; visceral pain;  Neuron-glial interaction;  Primary sensory ganglia