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 (∼25 %) of vagotomized NGNs displayed depolarizing after‐potentials (DAPs), not present in control NGNs. DAPs were inhibited by niflumic acid (125 μ m ) or cadmium (100 μ m ), 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 m m 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 n m ( n = 19 ; P = 0.44 ), respectively. Blocking CICR with 10 μ m ryanodine reduced DAP amplitude by ∼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.