Currents carried by L-, N and P/Q type calcium channels do not account for the total calcium current in myenteric neurons. This study identified all calcium channels expressed by guinea-pig small intestinal myenteric neurons maintained in primary culture. Calcium currents were recorded using whole-cell techniques. Depolarizations (holding potential = -70 mV) elicited inward currents that were blocked by CdCl₂ (100 µM). Combined application of nifedipine (blocks L-type channels), -conotoxin GVIA (blocks N-type channels) and -agatoxin IVA (blocks P/Q-type channels) inhibited calcium currents by 56%. Subsequent addition of the R-type calcium channel antagonists, NiCl₂(50 µM) or SNX-482 (0.1 µM), abolished the residual calcium current. NiCl₂ or SNX-482 alone inhibited calcium currents by 46%. The activation threshold for R-type calcium currents was -30 mV, the half-activation voltage was -5.2 ± 5 mV and the voltage sensitivity was 17 ± 3 mV e/fold increase in the calcium current. R-type currents activated fully in 10 ms at 10 mV. R-type calcium currents inactivated in 1 s at +10 mV and they inactivated (voltage sensitivity of 16 ± 1 mV) with a half-inactivation voltage of -76 ± 5 mV. These studies have accounted for all of the calcium channels in myenteric neurons. The data indicate that R-type calcium channels make the largest contribution to the total calcium current in myenteric neurons. The relatively positive half-activation voltage and rapid activation kinetics suggest that R-type channels could contribute to calcium entry during somal action potentials or during action potential-induced neurotransmitter release.