Systemic inflammation activates satellite glial cells in the mouse nodose ganglion and alters their functions.

Satellite glial cell (SGCs) in trigeminal and dorsal root ganglia are altered structurally and functionally under pathological conditions associated with chronic pain. These changes include reactive gliosis, augmented coupling by gap junctions, and increased responses to ATP via purinergic P2 receptors. Similar information for nodose ganglia (NG), which receive sensory inputs from internal organs via the vagus nerves, is missing. Here, we investigated changes in SGCs in mouse NG after the intraperitoneal administration of lipopolysaccharide (LPS), which induces systemic inflammation. Using calcium imaging we found that SGCs in intact, freshly isolated NG are sensitive to ATP, acting largely via purinergic P2 receptors (mixed P2X and P2Y), with threshold at 0.1 μM. A single systemic injection of LPS (2.5 mg/kg) induced a 6-fold increase in the responses to ATP, largely by augmenting the sensitivity of P2X receptors. Immunohistochemical analysis revealed that at 1-14 days post-LPS injection the expression of glial fibrillary acidic protein in SGCs was 2-3-fold greater than controls. The expression of pannexin 1 channels increased 2-fold at day 7 after LPS injection. Using intracellular labeling we examined dye coupling among SGCs around different neurons, and observed an over 2-fold higher incidence of dye coupling after the induction of inflammation. Incubating the ganglia with ATP increased dye coupling by acting on neuronal P2X receptors, suggesting a role for ATP in the LPS-induced changes. We conclude that inflammation induces prominent changes in SGCs of NG, which might have a role in vagal afferent functions, such as the inflammatory reflex. GLIA 2015;63:2121-2132.