Abstract
1. Cultured dorsal root ganglion cells of the bullfrog were voltage-clamped in the whole-cell configuration. 2. An adenosine 3':5'-cyclic monophosphate (cyclic AMP)-dependent cationic inward rectifier (IH) was inhibited by bath application of enflurane (0.2-0.8 mM) and halothane (0.2-0.5 mM), which thereby induced an outward current at the resting potential, and a membrane hyperpolarization in unclamped cells. 3. The main effect of enflurane (0.5 mM) was to displace the steady-state IH activation curve to a hyperpolarizing direction by about 10 mV, as well as to reduce the maximum H-conductance to about 20%. 4. Forskolin (1-10 microM), which enhances IH by producing a depolarizing shift in the IH activation curve and increasing the maximum H-conductance, recruited IH even when the current had already been eliminated by enflurane (1 mM).
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