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]

Armstrong CM. (2006). Na channel inactivation from open and closed states. Proceedings of the National Academy of Sciences of the United States of America. 103 [PubMed]

Balbi P, Martinoia S, Massobrio P. (2015). Axon-somatic back-propagation in detailed models of spinal alpha motoneurons. Frontiers in computational neuroscience. 9 [PubMed]

• Axon-somatic back-propagation in a detailed model of cat spinal motoneuron (Balbi et al, 2015) [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]

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]

Lee SC, Hayashida Y, Ishida AT. (2003). Availability of low-threshold Ca2+ current in retinal ganglion cells. Journal of neurophysiology. 90 [PubMed]

• Availability of low-threshold Ca2+ current in retinal ganglion cells (Lee SC et al. 2003) [Model]

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]

Mercer JN, Chan CS, Tkatch T, Held J, Surmeier DJ. (2007). Nav1.6 sodium channels are critical to pacemaking and fast spiking in globus pallidus neurons. The Journal of neuroscience : the official journal of the Society for Neuroscience. 27 [PubMed]

• Nav1.6 sodium channel model in globus pallidus neurons (Mercer et al. 2007) [Model]

Migliore M. (1996). Modeling the attenuation and failure of action potentials in the dendrites of hippocampal neurons. Biophysical journal. 71 [PubMed]

• CA1 Pyramidal Neuron: slow Na+ inactivation (Migliore 1996) [Model]

Powers RK, Elbasiouny SM, Rymer WZ, Heckman CJ. (2012). Contribution of intrinsic properties and synaptic inputs to motoneuron discharge patterns: a simulation study. Journal of neurophysiology. 107 [PubMed]

• Simulations of motor unit discharge patterns (Powers et al. 2011) [Model]

Raman IM, Bean BP. (2001). Inactivation and recovery of sodium currents in cerebellar Purkinje neurons: evidence for two mechanisms. Biophysical journal. 80 [PubMed]

• Cerebellar Purkinje Cell: resurgent Na current and high frequency firing (Khaliq et al 2003) [Model]

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]

Shapiro NP, Lee RH. (2007). Synaptic amplification versus bistability in motoneuron dendritic processing: a top-down modeling approach. Journal of neurophysiology. 97 [PubMed]