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ClC-2 channels regulate neuronal excitability, not intracellular Cl- levels (Ratte & Prescott 2011)
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This is the readme for the model files for the paper: Ratte S, Prescott SA (2011) ClC-2 Channels Regulate Neuronal Excitability, Not Intracellular Chloride Levels J Neurosci 31(44):15838-15843 These model files were supplied by Dr Steve Prescott. ClC2-VClamp-Prescott.ode implements simulations in voltage clamp. Data presented in Figure 1 of the paper can be reproduced using this model ClC2-IClamp-Prescott.ode implements simulations in current clamp. Data presented in Figures 2 and 3 of the paper can be reproduced using this model. The model is for a generic, single compartment neuron with multiple ion currents. The most notable mechanisms include ClC-2 (a rectifying chloride-leak channel) and KCC2 (potassium chloride co-transporter 2). A significant feature of the model is that it tracks intracellular chloride concentration. Moreover, the GABA-A receptor is modeled as passing both chloride and bicarbonate ions, which is important for proper calculation of the GABA reversal potential. Ornstein-Unlenbeck processes to simulate synaptic inhibition and excitation are also included.
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ClC-2 channels regulate neuronal excitability, not intracellular Cl- levels (Ratte & Prescott 2011)
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