Dynamic regulation of calcium influx by G-proteins, action potential waveform, and neuronal firing frequency - PubMed (original) (raw)
Pharmacological characterization of APW-evoked Ca2+ currents. A, B, Superimposed inward currents evoked by APWs (left) or rectangular pulses (to 0 mV, right) delivered from a holding potential of −80 mV before (CON), after a 3 min application of saturating ω-conotoxin GVIA (A), or during the application of 300 μ
m
Cd2+ (B). C, Concentration–response relationships for ω-conotoxin GVIA, Cd2+, and Ni2+ (as marked,n = 3–6 cells per point). Smooth lines represent the least-squares fits to a single binding site equation, % inhibition = (_I_max · [Inh])/([Inh] + IC50), where_I_max is the maximum inhibition, [Inh] the inhibitor concentration, and IC50 the concentration of inhibitor producing half-maximal blockade. Toxin was applied for the times necessary to approach equilibrium binding; concentrations of 0.03, 0.1, 0.3, 1.0, and 4.0 μ
m
were applied for 20, 20, 6.6. 6.5, and 2 min, respectively. In cells receiving prolonged toxin applications, currents were corrected for rundown (measured in control cells from the same plating at ∼1%/min).