Table 5.
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 | Vm–Iadap coupling |
IK−slow ↓ and INa−p ↑ | Resonance | Vm–Iadap 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).