Communication between neurons and glia in the dorsal root ganglia (DRG) and the central nervous system (CNS) is critical for nociception. Both Glial activation and proinflammatory cytokine induction underlie this communication. We investigated whether satellite glial cell (SGCs) and tumor necrosis factor alpha (TNF-α) activation in DRG participate 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 to 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 (10μg/kg per day). Based on our findings, TNF-α and SGC activation in neuron-glial communication of DRG and are critical in inflammatory visceral hyperalgesia.