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. 2018 Dec 3;12:88. doi: 10.3389/fninf.2018.00088

Table 5.

Correspondence between subcellular mechanisms that generated specific electrophysiological properties and how they were simplified in E-GLIF model elements.

Ionic channel mechanisms Electrophysiological property E-GLIF mechanisms
INa−t ↑ / IK−V ↓ balance Action potential Digital
Ih ↑INa−p ↑ / IK−slow ↓ balanceICa−HVA ↑/ IK−AHP ↓ balance Autorhythmicity Ie ↑/ Iadap↓ balance
INa−r ↑ and IK−A Depolarization-induced burst Idep
ICa−HVA ↑/ IK−AHP ↓ balanceIK−slow Spike-frequency adaptation Iadap
ICa−HVA ↑/ IK−AHP ↓ balance Phase-reset Iadap
Ih ↑ICa−LVA Post-inhibitory rebound burst Iadap ↑ and Idep
IK−slow ↓ and INa−p Subthreshold oscillations VmIadap coupling
IK−slow ↓ and INa−p Resonance VmIadap coupling

The arrow indicate depolarizing (↑) and hyperpolarizing (↓) actions of the membrane currents in the real cell and models. INa−t: transient sodium current; IK−V: delayed rectifier potassium current; Ih: hyperpolarization-activated current; INa−p: persistent sodium current; IK−slow: slow M-like potassium current; ICa−HVA: high voltage-activated calcium current; IK−AHP: SK-type calcium-dependent potassium current; INa−r: resurgent sodium current; IK−A: A-type potassium current; definitions and properties of the ionic currents are given in (Forti et al., 2006; Solinas et al., 2007a,b).