By David Rosenbaum
Presents an n-depth examine of the theoretical and engineering rules in the back of the tools and applied sciences used to unravel difficulties in experimental and scientific cardiac electrophysiology. every one bankruptcy supplies an intensive description of the rules underlying an easy strategy or expertise and illustrates the way it may be utilized to resolve difficulties in simple learn and the scientific surroundings.
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Extra info for Quantitative Cardiac Electrophysiology
Example text
From Ref. ) 34 Bett and Rasmusson The modeled current during certain simple protocols, such as reproducing an action potential, is insensitive to the whether the voltage dependence of inactivation is direct or indirect. However, when predicting the current due to conformation-specific drug binding, the exact description of the energetics of a particular state may be crucial. Regardless of the similarity of predicted currents, HH-like models with intrinsically voltagedependent inactivation can lead to significant differences in the predicted drug-binding behavior when compared with voltage-insensitive partially coupled (PC) models of inactivation.
Holding potential À60 mV. (B) The kinetics of association at repolarized holding potentials of À60 and À90 mV. (C) Voltage dependence of association kinetics. (From Ref. ) 34 Bett and Rasmusson The modeled current during certain simple protocols, such as reproducing an action potential, is insensitive to the whether the voltage dependence of inactivation is direct or indirect. However, when predicting the current due to conformation-specific drug binding, the exact description of the energetics of a particular state may be crucial.
In a Hodgkin-Huxley type of model, this is dealt with by adding several gating particles with differing time constants. In reality, modes of inactivation can be coupled, in a similar way to the coupling of inactivation with activation. A relatively slow type of inactivation resulting from changes in conformation at the extracellular mouth of the channel [112] is called C-type inactivation, after the C-terminal splice variant Shaker potassium channel in which it was first seen [113,114]. The molecular basis of C-type inactivation is not as well understood as N-type is.
