Gastrointestinal (GI)
pain is a common clinical problem, for which effective
therapy is quite limited. Sensations from the GI tract, including
pain, are mediated largely by neurons in the dorsal root ganglia (DRG), and to a smaller extent by vagal afferents emerging from neurons in the nodose/jugular ganglia. Neurons in rodent DRG become hyperexcitable in models of GI
pain (e.g., gastric or colonic
inflammation), and can serve as a source for
chronic pain. Glial cells are another
element in the
pain signaling pathways, and there is evidence that spinal glial cells (microglia and astrocytes) undergo activation (
gliosis) in various
pain models and contribute to
pain. Recently it was found that satellite glial cells (SGCs), the main type of glial cells in sensory ganglia, might also contribute to
chronic pain in rodent models. Most of that work focused on
somatic pain, but in several studies GI
pain was also investigated, and these are discussed in the present review. We have shown that colonic
inflammation induced by
dinitrobenzene sulfonic acid (
DNBS) in mice leads to the activation of SGCs in DRG and increases gap junction-mediated coupling among these cells. This coupling appears to contribute to the hyperexcitability of DRG neurons that innervate the colon. Blocking gap junctions (GJ) in vitro reduced neuronal hyperexcitability induced by
inflammation, suggesting that glial GJ participate in SGC-neuron interactions. Moreover, blocking GJ by
carbenoxolone and other agents reduces
pain behavior. Similar changes in SGCs were also found in the mouse nodose ganglia (NG), which provide sensory innervation to most of the GI tract. Following systemic
inflammation, SGCs in these ganglia were activated, and displayed augmented coupling and greater sensitivity to the
pain mediator
ATP. The contribution of these changes to
visceral pain remains to be determined. These results indicate that although
visceral pain is unique, it shares basic mechanisms with
somatic pain, suggesting that therapeutic approaches to both
pain types may be similar. Future research in this field should include additional types of GI injury and also other types of
visceral pain.