CA1 pyramidal neuron: rebound spiking (Ascoli et al.2010)

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Accession:126776
The model demonstrates that CA1 pyramidal neurons support rebound spikes mediated by hyperpolarization-activated inward current (Ih), and normally masked by A-type potassium channels (KA). Partial KA reduction confined to one or few branches of the apical tuft may be sufficient to elicit a local spike following a train of synaptic inhibition. These data suggest that the plastic regulation of KA can provide a dynamic switch to unmask post-inhibitory spiking in CA1 pyramidal neurons, further increasing the signal processing power of the CA1 synaptic microcircuitry.
Reference:
1 . Ascoli GA, Gasparini S, Medinilla V, Migliore M (2010) Local Control of Post-Inhibitory Rebound Spiking in CA1 Pyramidal Neuron Dendrites J.Neurosci. 30(18):6434-42 [PubMed]
Model Information (Click on a link to find other models with that property)
Model Type: Dendrite;
Brain Region(s)/Organism: Hippocampus;
Cell Type(s): Hippocampus CA1 pyramidal cell;
Channel(s): I Na,t; I A; I h; I Potassium;
Gap Junctions:
Receptor(s): Gaba;
Gene(s):
Transmitter(s): Gaba;
Simulation Environment: NEURON;
Model Concept(s): Action Potential Initiation; Activity Patterns; Dendritic Action Potentials; Active Dendrites; Detailed Neuronal Models; Action Potentials; Intrinsic plasticity; Synaptic Integration;
Implementer(s): Migliore, Michele [Michele.Migliore at Yale.edu];
Search NeuronDB for information about:  Hippocampus CA1 pyramidal cell; Gaba; I Na,t; I A; I h; I Potassium; Gaba;
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rebound
readme.html
h.mod
kadist.mod *
kaprox.mod *
kdrca1.mod *
na3n.mod *
naxn.mod *
4-ap.jpg
4-ap_plus_zd.jpg
control.jpg
fixnseg.hoc *
mod_func.c
mosinit.hoc
pc2b.hoc *
rebound.hoc
rebound.ses
                            
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