Ca2+ current in rabbit carotid body Glomus cells is conducted by multiple types of high-voltage-activated Ca2+ channels

Carotid bodies are sensory organs that detect changes in arterial oxygen. Glomus cells are presumed to be the initial sites for sensory transduction, and Ca2+-dependent neurotransmitter release from glomus cells is believed to be an obligatory step in this response. Some information exists on the Ca2+ channels in rat glomus cells. However, relatively Little is known about the types of Ca2+ channels present in rabbit glomus cells, the species in which most of the neurotransmitter release studies have been performed. Therefore we tested the effect of specific Ca2+ channel blockers on current recorded from freshly dissociated, adult rabbit carotid body glomus cells using the whole cell configuration of the patch-clamp technique. Macroscopic Ba2+ current elicited from a holding potential of -80 mV activated at a V-m of approximaely -30 mV, peaked between 0 and +10 mV and did not inactivate during 25-ms steps to positive test potentials. Prolonged (approximate to 2 min) depolarized holding potentials inactivated the current with a V-1/2 of -47 mV. There was no evidence for T-type channels. On steps to 0 mV, 6 mM Co2+ decreased peak inward current by 97 +/- 1% (mean +/- SE). Nisoldipine (2 mu M), 1 mu M omega-conotoxin GVIA, and 100 nM omega-agatoxin IVa each blocked a portion of the macroscopic Ca2+ current (30 +/- 5, 33 +/- 5, and 19 +/- 3% after rundown correction, respectively). Simultaneous application of these blockers revealed a resistant current that was not affected by 1 mu M omega-conotoxin MVIIC. This resistant current constituted 27 +/- 5% of the total macroscopic Ca2+ current. Each blocker had an effect in every cell so tested. However, the relative proportion of current blocked varied from cell to cell. These results suggest that L, N, P, and resistant channel types each conduct a significant proportion of the macroscopic Ca2+ current in rabbit glomus cells. Hypoxia-induced neurotransmitter release from glomus cells may involve one or more of these channels.