Fig. 1. Racemic ketamine reversibly inhibits nicotinic acetylcholine receptors (nAChRs;top left ) and K channels (top right ) present in the same membrane with different potencies. Current recordings show currents induced by acetylcholine (1 mm) under control conditions, during the application of ketamine (3 μm), and after washout of the drug. K currents were recorded by depolarizing the membrane from a holding potential of −80 mV to +40 mV. Shown are the K currents under control condition, during the ketamine effect (300 μm), and after washout of the drug. Concentration-dependent effects on nAChRs were described mathematically by a Hill function. The concentration for half-maximal inhibition was 1.4 μm; the Hill coefficient was −0.7. A complete concentration–response curve for K current inhibition was not obtained because data already existed:13IC50= 361 ± 39 μm; Hill coefficient = 0.9 ± 0.1 (mean ± SEM).

Fig. 1. Racemic ketamine reversibly inhibits nicotinic acetylcholine receptors (nAChRs;top left ) and K channels (top right ) present in the same membrane with different potencies. Current recordings show currents induced by acetylcholine (1 mm) under control conditions, during the application of ketamine (3 μm), and after washout of the drug. K currents were recorded by depolarizing the membrane from a holding potential of −80 mV to +40 mV. Shown are the K currents under control condition, during the ketamine effect (300 μm), and after washout of the drug. Concentration-dependent effects on nAChRs were described mathematically by a Hill function. The concentration for half-maximal inhibition was 1.4 μm; the Hill coefficient was −0.7. A complete concentration–response curve for K current inhibition was not obtained because data already existed:13IC50= 361 ± 39 μm; Hill coefficient = 0.9 ± 0.1 (mean ± SEM).

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