These mod files supplied by Dr Raman are for the below two references. ... we modeled action potential firing by simulating eight currents directly recorded from Purkinje cells in both wild-type and (mutant) med mice. Regular, high-frequency firing was slowed in med Purkinje neurons. In addition to disrupted sodium currents, med neurons had small but significant changes in potassium and leak currents. Simulations indicated that these modified non-sodium currents could not account for the reduced excitability of med cells but instead slightly facilitated spiking. The loss of NaV1.6-specific kinetics, however, slowed simulated spontaneous activity. Together, the data suggest that across a range of conditions, sodium currents with a resurgent component promote and accelerate firing. See papers for more and details.
Model Type: Neuron or other electrically excitable cell
Cell Type(s): Cerebellum Purkinje GABA cell
Currents: I Na,t; I K; I h; I K,Ca; I Sodium; I Calcium; I Potassium
Genes: Nav1.6 SCN8A
Model Concept(s): Activity Patterns; Ion Channel Kinetics; Action Potentials
Simulation Environment: NEURON
Implementer(s): Raman, Indira M [i-raman at northwestern.edu]; Bean, Bruce [bruce_bean at hms.harvard.edu]; Gouwens, Nathan W [nathan_gouwens at hms.harvard.edu]
References:
Khaliq ZM, Gouwens NW, Raman IM. (2003). The contribution of resurgent sodium current to high-frequency firing in Purkinje neurons: an experimental and modeling study. The Journal of neuroscience : the official journal of the Society for Neuroscience. 23 [PubMed]
Raman IM, Bean BP. (2001). Inactivation and recovery of sodium currents in cerebellar Purkinje neurons: evidence for two mechanisms. Biophysical journal. 80 [PubMed]