Fig. 2. S  (+)-ketamine (top left ) and R  (−)-ketamine (top right ) reversibly inhibit nicotinic acetylcholine receptors (nAChRs). Recordings show currents induced by acetylcholine (1 mm) under control conditions, during the application of S  (+)-ketamine (10 μm) and R  (−)-ketamine (10 μm), and after the washout of the drugs. The IC50value for current inhibition by the S  (+)-isomer was three- to fourfold lower than that of the R  (−)-isomer. Concentration-dependent effects on nAChRs were described mathematically by Hill functions. The parameters of the Hill function for the S  (+)-isomer were as follows: IC50value = 0.92 μm, Hill coefficient =−0.7; for the R  (−)-isomer: IC50value = 3.6 μm, Hill coefficient =−0.9. The IC50values for nAChR inhibition significantly differed between the S  (+)- and the R  (−)-isomer.

Fig. 2. S  (+)-ketamine (top left ) and R  (−)-ketamine (top right ) reversibly inhibit nicotinic acetylcholine receptors (nAChRs). Recordings show currents induced by acetylcholine (1 mm) under control conditions, during the application of S  (+)-ketamine (10 μm) and R  (−)-ketamine (10 μm), and after the washout of the drugs. The IC50value for current inhibition by the S  (+)-isomer was three- to fourfold lower than that of the R  (−)-isomer. Concentration-dependent effects on nAChRs were described mathematically by Hill functions. The parameters of the Hill function for the S  (+)-isomer were as follows: IC50value = 0.92 μm, Hill coefficient =−0.7; for the R  (−)-isomer: IC50value = 3.6 μm, Hill coefficient =−0.9. The IC50values for nAChR inhibition significantly differed between the S  (+)- and the R  (−)-isomer.

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