Afferent nerve fibers from the kidneys are putatively involved in renal inflammation by controlling sympathetic nerve activity and secretion of neuropeptides (SP, CGRP). TRPV1-induced CGRP release from cutaneous neurons is reported to be much higher in C57BL/6 than in AKR mice (Mogil et al. 2005, PNAS). We wanted to test whether this strain difference also applies to renal dorsal root ganglion (DRG) neurons and to their sensitization by systemic inflammation of the donor animals.

DRG neurons (T11-L2) in primary culture which were retrogradely labeled from the kidneys were investigated by whole- cell patch-clamping. TRPV1 currents were identified by superfusion with 1 mM capsaicin. Acute renal failure was induced by endotoxemia using lipopolysaccharide (LPS) injection 24 h prior to euthanasia.

Capsaicin-induced currents were mainly observed in small to medium-sized renal DRG neurons. In AKR mice only 29% of these neurons were capsaicin-sensitive whereas C57BL/6 mice showed 60% responsiveness and more than 5-fold greater mean peak currents. The LPS model of renal failure did not change capsaicin sensitivity, neither in C57BL/6 nor in AKR mice.

The hereditary strain difference in capsaicin responsiveness was fully confirmed for renal sensory neurons, but the systemic inflammation did not alter this parameter to a measurable extent.