CHARACTERIZATION OF CALCIUM CURRENTS IN AORTIC BARORECEPTOR NEURONS

1. Calcium currents in identified rat aortic baroreceptors were characterized with the perforated patch whole-cell voltage-clamp technique. Aortic baroreceptors were distinguished from other neurons by the presence of a fluorescent tracer that was previously applied to the aortic depressor nerve. The diversity of calcium currents in unidentified neurons dissociated from neonatal rat nodose ganglia were also examined. 2. A population of aortic baroreceptors (63%, 7 of 11) possessed a low-threshold, also referred to as a T-type, calcium current. This current was typically < 100 pA in 2 mM Ca [72.7 +/- 20. 9 (SE) pA, n = 71, had a rapid activation and inactivation, and inactivated completely at conditioning voltages positive to -50 mV. 3. All aortic baroreceptors possessed high-threshold calcium currents that were activated at voltages positive to -30 mV, with typical maximum amplitudes of 600-1,000 pA (826 +/- 79 pA, n = 11). 4. The high-threshold current inactivated with three exponential rates of decay of tau = 10.7 +/- 2.2 ms, 138 +/- 14.6 ms, and a third tau > 3 s. It was not possible to separate the kinetic components of inactivation with conditioning voltages (voltage-dependent inactivation), activation thresholds, deactivation kinetics, or calcium-channel antagonists. 5. The voltage-dependent inactivation of high-threshold calcium cur-rents began at voltages positive to -70 mV and became steeply voltage dependent between -60 and -10 mV. Unexpectedly, the three decay constants were present after all conditioning voltages. There were no conditioning voltages that excluded any component. 6. Omega-Conotoxin (GVIA) blocked -70% of the high-threshold current and inhibited all kinetic components of inactivation equally. Omega-Conotoxin (1-mu-M) inhibited the magnitude of calcium current activated after each conditioning voltage without any change in the voltage dependence of inactivation. The dihydropyridine antagonist nimodipine (2-mu-M) had little or no effect. 7. Analysis of tail currents indicated that high-threshold calcium currents activate at voltages positive to -30 mV. Omega-Conotoxin inhibited the tail currents but did not alter the threshold or range of voltages over which activation occurred. 8. High-threshold tail currents deactivated with a single exponential rate after different test voltages and varying duration. 9. In conclusion, the calcium currents in aortic baroreceptors have been characterized. A population of aortic baroreceptors possess a low-threshold (T-type) calcium current. All aortic baroreceptors possess high-threshold calcium currents that inactivate with three rates of decay. The entire high-threshold calcium current profile activated at voltages positive to -30 mV, inactivated after conditioning voltages positive to -70 mV, and deactivated with a single rate of decay, was insensitive to nimodipine, and was blocked (70%) by omega-conotoxin.