Andreozzi E, Carannante I, D'Addio G, Cesarelli M, Balbi P. (2019). Phenomenological models of NaV1.5. A side by side, procedural, hands-on comparison between Hodgkin-Huxley and kinetic formalisms Scientific reports. 9 [PubMed]

• Phenomenological models of NaV1.5: Hodgkin-Huxley and kinetic formalisms (Andreozzi et al 2019) [Model]

Balbi P, Massobrio P, Hellgren Kotaleski J. (2017). A single Markov-type kinetic model accounting for the macroscopic currents of all human voltage-gated sodium channel isoforms. PLoS computational biology. 13 [PubMed]

• A single kinetic model for all human voltage-gated sodium channels (Balbi et al, 2017) [Model]

Baranauskas G, Martina M. (2006). Sodium currents activate without a Hodgkin-and-Huxley-type delay in central mammalian neurons. The Journal of neuroscience : the official journal of the Society for Neuroscience. 26 [PubMed]

• Sodium currents activate without a delay (Baranauskas and Martina 2006) [Model]

Clay JR, Paydarfar D, Forger DB. (2008). A simple modification of the Hodgkin and Huxley equations explains type 3 excitability in squid giant axons. Journal of the Royal Society, Interface. 5 [PubMed]

• Model of Type 3 firing in neurons (Clay et al 2008) [Model]

Deister CA, Chan CS, Surmeier DJ, Wilson CJ. (2009). Calcium-activated SK channels influence voltage-gated ion channels to determine the precision of firing in globus pallidus neurons. The Journal of neuroscience : the official journal of the Society for Neuroscience. 29 [PubMed]

• Model of SK current`s influence on precision in Globus Pallidus Neurons (Deister et al. 2009) [Model]

Gurkiewicz M, Korngreen A. (2007). A numerical approach to ion channel modelling using whole-cell voltage-clamp recordings and a genetic algorithm. PLoS computational biology. 3 [PubMed]

• Ion channel modeling with whole cell and a genetic algorithm (Gurkiewicz and Korngreen 2007) [Model]

Gurkiewicz M, Korngreen A, Waxman SG, Lampert A. (2011). Kinetic modeling of Nav1.7 provides insight into erythromelalgia-associated F1449V mutation. Journal of neurophysiology. 105 [PubMed]

• HMM of Nav1.7 WT and F1449V (Gurkiewicz et al. 2011) [Model]

Hennings K, Arendt-Nielsen L, Andersen OK. (2005). Breakdown of accommodation in nerve: a possible role for persistent sodium current. Theoretical biology & medical modelling. 2 [PubMed]

• Breakdown of accmmodation in nerve: a possible role for INAp (Hennings et al 2005) [Model]

Kahlig KM, Misra SN, George AL. (2006). Impaired inactivation gate stabilization predicts increased persistent current for an epilepsy-associated SCN1A mutation. The Journal of neuroscience : the official journal of the Society for Neuroscience. 26 [PubMed]

Menon V, Spruston N, Kath WL. (2009). A state-mutating genetic algorithm to design ion-channel models. Proceedings of the National Academy of Sciences of the United States of America. 106 [PubMed]

• Hippocampus CA1 pyramidal model with Na channel exhibiting slow inactivation (Menon et al. 2009) [Model]

Patel SP, Campbell DL. (2005). Transient outward potassium current, 'Ito', phenotypes in the mammalian left ventricle: underlying molecular, cellular and biophysical mechanisms. The Journal of physiology. 569 [PubMed]

Sangrey TD, Friesen WO, Levy WB. (2004). Analysis of the optimal channel density of the squid giant axon using a reparameterized Hodgkin-Huxley model. Journal of neurophysiology. 91 [PubMed]

Schwarz JR, Reid G, Bostock H. (1995). Action potentials and membrane currents in the human node of Ranvier. Pflugers Archiv : European journal of physiology. 430 [PubMed]

• Peripheral nerve:Morris-Lecar implementation of (Schwarz et al 1995) [Model]

Thomas EA, Petrou S. (2013). Network-specific mechanisms may explain the paradoxical effects of carbamazepine and phenytoin. Epilepsia. 54 [PubMed]

• State dependent drug binding to sodium channels in the dentate gyrus (Thomas & Petrou 2013) [Model]

Wang S et al. (2005). Time- and voltage-dependent components of Kv4.3 inactivation. Biophysical journal. 89 [PubMed]