Electrophysiological responses of dissociated type I cells of the rabbit carotid body to cyanide.

1. The carotid body is the major peripheral sensor of arterial PO2 in the mammal and is excited by cyanide (CN‐). Type I cells, the presumed sites for transduction, were freshly dissociated from the carotid body of the adult rabbit and studied with the whole‐cell patch clamp technique. 2. Type I cells were hyperpolarized by CN‐, the action potential was shortened, and there was an increased after‐hyperpolarization. 3. Under voltage clamp control, CN‐ increased a voltage‐dependent outward current, which showed pronounced outward rectification. Tail currents increased by CN‐ reversed close to the predicted EK, the reversal potential of the CN‐‐induced current depended on extracellular [K+], and the current was blocked by intracellular TEA+ and Cs+. 4. The i‐V relation of the CN‐‐induced conductance strongly mirrored that of voltage‐gated Ca2+ entry, and the response was abolished by removal of extracellular Ca2+. We conclude that the increased gK is Ca2+ ‐dependent (gK(Ca]. 5. The Ca2+ current was attenuated by CN‐, and showed an increased rate of inactivation. Thus, the increased gK(Ca) must result from an alteration in Ca2+ homeostasis independent of the Ca2+ current, and not an increased Ca2+ entry through voltage‐activated channels. 6. Carbachol also hyperpolarized cells and increased a K+ conductance. 7. At depolarized holding potentials a steady‐state outward current was increased by CN‐. The current reversed close to EK, and was associated with increased current fluctuations. Noise analysis showed that a channel conductance of 3 pS carries the current. 8. The response to CN‐ was not impaired by the inclusion of 5 mM‐MgATP in the patch pipette. 9. If signals to the CNS are initiated by the calcium‐dependent release of transmitters from type I cells, transduction would appear to be the direct consequence of the energy dependence of Ca2+ homeostasis.