Properties of aconitine-induced block of KDR current in NG108-15 neurons (Lin et al. 2008)

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"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."
1 . Lin MW, Wang YJ, Liu SI, Lin AA, Lo YC, Wu SN (2008) Characterization of aconitine-induced block of delayed rectifier K+ current in differentiated NG108-15 neuronal cells. Neuropharmacology 54:912-23 [PubMed]
Model Information (Click on a link to find other models with that property)
Model Type: Neuron or other electrically excitable cell;
Brain Region(s)/Organism:
Cell Type(s): Neuroblastoma;
Channel(s): I K; I Sodium; I Potassium; I_KHT;
Gap Junctions:
Simulation Environment: XPPAUT;
Model Concept(s): Ion Channel Kinetics; Simplified Models; Action Potentials; Methods;
Implementer(s): Wu, Sheng-Nan [snwu at]; Lin, Ming-Wei ; Wan, Ya-Jean ; Lin, An-An ;
Search NeuronDB for information about:  I K; I Sodium; I Potassium; I_KHT;
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