Recently, we found that renal afferent neurons exhibit predominantly tonic firing pattern upon depolarizing current injection, most likely due to specific expression of voltage gated sodium channels. In pathophysiological states associated with increased efferent nerve activity, the role of these neurons is unclear. With this study we aim to investigate the firing patterns of renal afferent neurons in an in vitro model of inflammation.

Labeling (DiI) allows the identification of dorsal root ganglion (DRG) neurons with projection to the kidney. DRG neurons (Th₁₁-L₂)were incubated with the chemokine CXCL1 (1,5nmol/ml) for 12 hours before patch clamp recordings. Current clamp was used to characterize neurons as "tonic", i.e. sustained action potential (AP) firing or "phasic", i.e. <5 APs according to their firing response to depolarizing current injections. Firing threshold, overshoot and AP-duration was determined in renal and non-renal neurons incubated with CXCL1, compared to controls.

Renal neurons exposed to CXCL1 show a significant decrease of tonic firing pattern compared to controls (35,6% vs. 57%).Tonic neurons exposed to CXCL1 exhibit no significant changes in action potential shape compared to controls. Phasic cells exposed CXCL1 showed a significantly higher overshoot, a lower firing threshold and shorter AP- duration than phasic controls.

In conclusion we found that renal afferent DRG neurons exhibit significantly less tonic firing pattern in an in vitro model of renal inflammation compared to control. AP changes in phasic neurons point to altered sodium channel expression might lead to a faster inactivation of theses channels and decreased firing activity.