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(Includes both p-type and q-type currents)
| Models | Description |
| A simplified cerebellar Purkinje neuron (the PPR model) (Brown et al. 2010) | |
| These models were implemented in NEURON by Sherry-Ann Brown in the laboratory of Leslie M. Loew. The files reproduce Figures 2c-f from Brown et al, 2010 "Virtual NEURON: a Strategy For Merged Biochemical and Electrophysiological Modeling". | |
| Axonal NaV1.6 Sodium Channels in AP Initiation of CA1 Pyramidal Neurons (Royeck et al. 2008) | |
| "... We show that the Na+ channel NaV1.6 displays a striking aggregation at the AIS of cortical neurons. ... In combination with simulations using a realistic computer model of a CA1 pyramidal cell, our results imply that a hyperpolarized voltage-dependence of activation of AIS NaV1.6 channels is important both in determining spike threshold and localizing spike initiation to the AIS. ... These results suggest that NaV1.6 subunits at the AIS contribute significantly to its role as spike trigger zone and shape repetitive discharge properties of CA1 neurons." | |
| Axonal gap junctions produce fast oscillations in cerebellar Purkinje cells (Traub et al. 2008) | |
| Examines how electrical coupling between proximal axons produces fast oscillations in cerebellar Purkinje cells. Traub RD, Middleton SJ, Knopfel T, Whittington MA (2008) Model of very fast (>75 Hz) network oscillations generated by electrical coupling between the proximal axons of cerebellar Purkinje cells. European Journal of Neuroscience in press. | |
| CA1 pyramidal neuron to study INaP properties and repetitive firing (Uebachs et al. 2010) | |
| A model of a CA1 pyramidal neuron containing a biophysically realistic morphology and 15 distributed voltage and Ca2+-dependent conductances. Repetitive firing is modulated by maximal conductance and the voltage dependence of the persistent Na+ current (INaP). | |
| Cerebellar purkinje cell (De Schutter and Bower 1994) | |
| Tutorial simulation of a cerebellar Purkinje cell. This tutorial is based upon a GENESIS simulation of a cerebellar Purkinje cell, modeled and fine-tuned by Erik de Schutter. The tutorial assumes that you have a basic knowledge of the Purkinje cell and its synaptic inputs. It gives visual insight in how different properties as concentrations and channel conductances vary and interact within a real Purkinje cell. | |
| Complex CA1-neuron to study AP initiation (Wimmer et al. 2010) | |
| Complex model of a pyramidal CA1-neuron, adapted from Royeck, M., et al. Role of axonal NaV1.6 sodium channels in action potential initiation of CA1 pyramidal neurons. Journal of neurophysiology 100, 2361-2380 (2008). It contains a biophysically realistic morphology comprising 265 compartments (829 segments) and 15 different distributed Ca2+- and/or voltage-dependent conductances. | |
| Dendritica (Vetter et al 2001) | |
| Dendritica is a collection of programs for relating dendritic geometry and signal propagation. The programs are based on those used for the simulations described in: Vetter, P., Roth, A. & Hausser, M. (2001) For reprint requests and additional information please contact Dr. M. Hausser, email address: m.hausser@ucl.ac.uk | |
| Effects of KIR current inactivation in NAc Medium Spiny Neurons (Steephen and Manchanda 2009) | |
| "Inward rectifying potassium (KIR) currents in medium spiny (MS) neurons of nucleus accumbens inactivate significantly in ~40% of the neurons but not in the rest, which may lead to differences in input processing by these two groups. Using a 189-compartment computational model of the MS neuron, we investigate the influence of this property using injected current as well as spatiotemporally distributed synaptic inputs. Our study demonstrates that KIR current inactivation facilitates depolarization, firing frequency and firing onset in these neurons. ..." | |
| Elementary mechanisms producing facilitation of Cav2.1 (P/Q-type) channels | |
| "The regulation of Ca(V)2.1 (P/Q-type) channels by calmodulin (CaM) showcases the powerful Ca(2+) decoding capabilities of CaM in complex with the family of Ca(V)1-2 Ca(2+) channels. Throughout this family, CaM does not simply exert a binary on/off regulatory effect; rather, Ca(2+) binding to either the C- or N-terminal lobe of CaM alone can selectively trigger a distinct form of channel modulation. ... Ca(2+) binding to the C-terminal lobe induces Ca(2+)-dependent facilitation of opening (CDF), whereas the N-terminal lobe yields Ca(2+)-dependent inactivation of opening (CDI). ... Furthermore, direct single-channel determinations of channel open probability (P(o)) and kinetic simulations demonstrate that CDF represents a genuine enhancement of open probability, without appreciable change of activation kinetics. This enhanced-opening mechanism suggests that the CDF evoked during action-potential trains would produce not only larger, but longer-lasting Ca(2+) responses, an outcome with potential ramifications for short-term synaptic plasticity." | |
| Synaptic integration in tuft dendrites of layer 5 pyramidal neurons (Larkum et al. 2009) | |
| Simulations used in the paper. Voltage responses to current injections in different tuft locations; NMDA and calcium spike generation. Summation of multiple input distribution. | |
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