Department of Gastroenterology, Ruijin Hospital, Shanghai Jiaotong University School of Medicine, Shanghai, China; and.
Am J Physiol Gastrointest Liver Physiol. 2014 May 1;306(9):G788-95. doi: 10.1152/ajpgi.00318.2013. Epub 2014 Mar 13.
Communication between neurons and glia in the dorsal root ganglia (DRG) and the central nervous system is critical for nociception. Both glial activation and proinflammatory cytokine induction underlie this communication. We investigated whether satellite glial cell (SGC) and tumor necrosis factor-α (TNF-α) activation in DRG participates in a 2,4,6-trinitrobenzene sulfonic acid (TNBS)-induced rat model of visceral hyperalgesia. In TNBS-treated rats, TNF-α expression increased in DRG and was colocalized to SGCs enveloping a given neuron. These SGCs were activated as visualized under electron microscopy: they had more elongated processes projecting into the connective tissue space and more gap junctions. When nerves attached to DRG (L6-S1) were stimulated with a series of electrical stimulations, TNF-α were released from DRG in TNBS-treated animals compared with controls. Using a current clamp, we noted that exogenous TNF-α (2.5 ng/ml) increased DRG neuron activity, and visceral pain behavioral responses were reversed by intrathecal administration of anti-TNF-α (10 μg·kg(-1)·day(-1)). Based on our findings, TNF-α and SGC activation in neuron-glial communication are critical in inflammatory visceral hyperalgesia.
背根神经节（DRG）和中枢神经系统中神经元和神经胶质之间的通讯对于伤害感受至关重要。胶质细胞的激活和促炎细胞因子的诱导是这种通讯的基础。我们研究了卫星胶质细胞（SGC）和肿瘤坏死因子-α（TNF-α）在 DRG 中的激活是否参与了 2,4,6-三硝基苯磺酸（TNBS）诱导的内脏痛觉过敏大鼠模型。在 TNBS 处理的大鼠中，DRG 中 TNF-α的表达增加，并与包裹特定神经元的 SGC 共定位。这些 SGC 如电子显微镜下所见被激活：它们具有更多伸向结缔组织空间的细长突起和更多的缝隙连接。当刺激与 DRG（L6-S1）相连的神经时，与对照组相比，来自 DRG 的 TNF-α在 TNBS 处理的动物中被释放。使用电流钳，我们注意到外源性 TNF-α（2.5ng/ml）增加了 DRG 神经元的活性，鞘内给予抗 TNF-α（10μg·kg(-1)·day(-1)）可逆转内脏痛觉行为反应。基于我们的发现，神经元-神经胶质通讯中 TNF-α和 SGC 的激活在炎症性内脏痛觉过敏中至关重要。
