Characterization of calcium currents in aortic baroreceptor neurons

Document Type

Journal Article

Publication Date

1-1-1992

Journal

Journal of Neurophysiology

Volume

68

Issue

2

DOI

10.1152/jn.1992.68.2.509

Abstract

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 = 7], 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 τ = 10.7 ± 2.2 ms, 138 ± 14.6 ms, and a third τ > 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 currents 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. ω-Conotoxin (GVIA) blocked ~70% of the high-threshold current and inhibited all kinetic components of inactivation equally. ω-Conotoxin (1 μM) 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 μM) had little or no effect. 7. Analysis of tail currents indicated that high-threshold calcium currents activate at voltages positive to -30 mV. ω-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 ω-conotoxin.

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