CA1 pyramidal neuron: Dendritic Na+ spikes are required for LTP at distal synapses (Kim et al 2015)

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Accession:184054
This model simulates the effects of dendritic sodium spikes initiated in distal apical dendrites on the voltage and the calcium dynamics revealed by calcium imaging. It shows that dendritic sodium spike promotes large and transient calcium influxes via NMDA receptor and L-type voltage-gated calcium channels, which contribute to the induction of LTP at distal synapses.
Reference:
1 . Kim Y, Hsu CL, Cembrowski MS, Mensh BD, Spruston N (2015) Dendritic sodium spikes are required for long-term potentiation at distal synapses on hippocampal pyramidal neurons. Elife [PubMed]
Model Information (Click on a link to find other models with that property)
Model Type: Neuron or other electrically excitable cell; Synapse; Channel/Receptor; Dendrite;
Brain Region(s)/Organism: Hippocampus;
Cell Type(s): Hippocampus CA1 pyramidal GLU cell;
Channel(s): I L high threshold; I K; Ca pump; I Sodium;
Gap Junctions:
Receptor(s): AMPA; NMDA;
Gene(s):
Transmitter(s): Glutamate;
Simulation Environment: NEURON;
Model Concept(s): Dendritic Action Potentials; Ion Channel Kinetics; Active Dendrites; Detailed Neuronal Models; Synaptic Plasticity; Long-term Synaptic Plasticity; Synaptic Integration; Calcium dynamics; Conductance distributions;
Implementer(s): Cembrowski, Mark S [cembrowskim at janelia.hhmi.org]; Hsu, Ching-Lung [hsuc at janelia.hhmi.org];
Search NeuronDB for information about:  Hippocampus CA1 pyramidal GLU cell; AMPA; NMDA; I L high threshold; I K; I Sodium; Ca pump; Glutamate;
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fullMorphCaLTP8
fullMorphCaLTP8
calH.mod
cdp.mod
id.mod
kad.mod *
kap.mod *
kdr.mod *
na3.mod *
nmdaSyn.mod
spgen2.mod
analyseTBSCC.hoc
channelParameters.hoc
displayPanels.hoc
doTBSStimCC.hoc
getVoltageIntegral.hoc
init.hoc
initializationAndRun.hoc
morphology_ri06.nrn *
naceaxon.nrn *
plotTBSCC.hoc
preallocate.hoc
resetNSeg.hoc *
runTBSCC.hoc
seclists.hoc
start.hoc
                            
////////////////////////////////////////////////////////////////////////////////
//
// A MODEL FOR eLife 2015;10.7554/eLife.06414 
// Yujin Kim*, Ching-Lung Hsu*, Mark Cembrowski, Brett Mensh, Nelson Spruston
//
// MODEL AUTHORS: Mark Cembrowski and Ching-Lung Hsu
//
// TO SUPPLEMENT EXPERIMENTS BY Yujin Kim and Ching-Lung Hsu
// For correspondence: Nelson Spruston 
// Janelia Research Campus, Howard Hughes Medical Institute
// July, 2015
//
////////////////////////////////////////////////////////////////////////////////

// LOAD GUI.
{
	load_file("nrngui.hoc")
}

// LOAD MORPHOLOGY RESETTING nseg AS NECESSARY; CREATE STIMULATING ELECTRODE
{
	xopen("morphology_ri06.nrn")	// pyramidal neuron geometry
	xopen("naceaxon.nrn")		// axon geometry (fake)
	load_file("resetNSeg.hoc")	// reset nseg as needed
}

// CREATE STIMULATING ELECTRODE
objref ppStim
{
	ppStim = new SpGen2(0.5)
}

// IMPLEMENT ION CHANNELS
{
	xopen("init.hoc")
}

// LOAD INITIALIZATION AND RUN ROUTINES
{
	load_file("initializationAndRun.hoc")
} 

// PREALLOCATE MEMORY
{
	load_file("preallocate.hoc")
}

print "\n\n\n" // make some space

//////////////////////////////////////////////////////////////////////////////////////////////////
// SELECT STIMULATION AND RECORDING CONFIGURATION: comment out the config that is not to be used
//////////////////////////////////////////////////////////////////////////////////////////////////

// DO A SINGLE TBS STIMULUS
{
	print "\tSimulating response to single high-frequency burst of TBS of the perforant path"
	
	xopen("doTBSStimCC.hoc")
}


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