"The effects of aconitine (ACO), a highly toxic alkaloid, on ion currents in differentiated NG108-15 neuronal cells were investigated in this study. ACO (0.3-30 microM) suppressed the amplitude of delayed rectifier K+ current (IK(DR)) in a concentration-dependent manner with an IC50 value of 3.1 microM. The presence of ACO enhanced the rate and extent of IK(DR) inactivation, although it had no effect on the initial activation phase of IK(DR). ... A modeled cell was designed to duplicate its inhibitory effect on spontaneous pacemaking. ... Taken together, the experimental data and simulations show that ACO can block delayed rectifier K+ channels of neurons in a concentration- and state-dependent manner. Changes in action potentials induced by ACO in neurons in vivo can be explained mainly by its blocking actions on IK(DR) and INa."
Model Type: Neuron or other electrically excitable cell
Cell Type(s): Neuroblastoma
Currents: I K; I Sodium; I Potassium; I_KHT
Model Concept(s): Ion Channel Kinetics; Simplified Models; Action Potentials; Methods
Simulation Environment: XPPAUT
Implementer(s): Wu, Sheng-Nan [snwu at mail.ncku.edu.tw]; Lin, Ming-Wei ; Wan, Ya-Jean ; Lin, An-An
References:
Lin MW et al. (2008). Characterization of aconitine-induced block of delayed rectifier K+ current in differentiated NG108-15 neuronal cells. Neuropharmacology. 54 [PubMed]