Calcium and calcium-activated currents in vagotomized rat primary vagal afferent neurons.

Adult inferior vagal ganglion neurons (nodose ganglion neurons, NGNs) were acutely isolated 4-6 days after section of their peripheral axons (vagotomy) and examined with the whole-cell patch-clamp technique. A subset (approximately 25 %) of vagotomized NGNs displayed depolarizing after-potentials (DAPs), not present in control NGNs. DAPs were inhibited by niflumic acid (125 microM) or cadmium (100 microM), and had a reversal potential near E(Cl), indicating that they were due to Ca(2+)-activated chloride current (I(Cl(Ca))). N-type, L-type, T-/R- and other types of voltage-dependent Ca(2+) channels provided about 43, 2, 16 and 40 % of the trigger Ca(2+) for DAP generation, respectively. Intracellular Ca(2+) concentration ([Ca(2+)](i)) was estimated using fura-2 fluorescence. Resting [Ca(2+)](i) and peak [Ca(2+)](i) elevation induced by activating Ca(2+)-induced Ca(2+) release (CICR) stores with 10 mM caffeine were not significantly different among control NGNs, vagotomized NGNs with DAPs and vagotomized NGNs without DAPs, averaging 54 +/- 7.9 (n = 19; P = 0.49) and 2022 +/- 1059 nM (n = 19; P = 0.44), respectively. Blocking CICR with 10 microM ryanodine reduced DAP amplitude by approximately 37 %. Ca(2+) influx induced by action potential waveforms was increased by over 250 % in vagotomized NGNs with DAPs (19.0 +/- 2.1 pC) compared to control NGNs (5.0 +/- 0.8 pC) or vagotomized NGNs without DAPs (7.0 +/- 0.8 pC). L-type, N-type, T-/R-type and other types of Ca(2+) influx were increased proportionately in vagotomized NGNs with DAPs. In conclusion, a subset of vagotomized NGNs have increased Ca(2+) currents and express I(Cl(Ca)). These NGNs respond electrically to increases in [Ca(2+)](i) during regeneration.