Propofol inhibited the delayed rectifier potassium current (Ik) via activation of protein kinase C epsilon in rat parietal cortical neurons

Propofol has been shown to exert neuroprotective effects. Delayed rectifier potassium current (IK) was reported to be closely related to neuronal damage. This study was designed to test the effects of propofol on IK in rat parietal cortical neurons and the involvement of PKC in this activity. Whole-cell patch-clamp recordings were performed in rat parietal cortical neurons. The amplitudes of IK were recorded before and after the addition of different concentrations of propofol. Propofol concentration-dependently inhibited IK with an IC50 value of 36.3 ± 2.7 μM. Moreover, propofol caused a downward shift of the I-V curve of IK in a concentration dependent manner. The kinetics of IK was altered by propofol, with decreased activation and delayed recovery of IK. Pretreatment with calphostin-C (a non-selective inhibitor of PKC) or PKC epsilon translocation inhibitor peptide (PKC epsilon inhibitor) abrogated the inhibition of IK by propofol. In conclusion, propofol inhibited IK via the activation of PKC epsilon in rat cerebral parietal cortical neurons.