Effect of ketamine on voltage-gated potassium channels in rat primary sensory cortex pyramidal neurons

Ketamine is an intravenous anesthetic commonly used in clinical, which has sedative and analgesic effects. Potassium channels exert many physiological functions in excitable cells. Therefore, potassium channels may be one of the targets of ketamine. In this study, we used patch clamp to study the effects of ketamine on voltage-gated potassium channels in primary sensory cortex (S1) neurons. We recorded the outward potassium currents (IA) and delayed rectifier potassium currents (IK) separately. We found that ketamine both concentration-dependently inhibited IA currents and IK currents in S1 neurons. Ketamine (100 and 300 μM) induced a concentration-dependent hyperpolarizing shift in V1/2, without affecting the slope factor (κ) or inactivation of IA. Ketamine induced a concentration-dependent hyperpolarizing shift in V1/2 of IK, without affecting its κ. Ketamine (100 and 300 μM) did not alter the steady-state activation or its κ. Hence, ketamine inhibits IA and IK in a concentration-dependent manner in S1 pyramidal neurons. The inactivation of IA does not appear to be involved in the inhibitory effect of ketamine on IA. Ketamine inhibits IK mainly by speeding up the inactivation of IK in S1 pyramidal neurons.