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
                            
ttxSoma = 0		// simulate 20nM TTX in bath?  0 = no; 1 = yes

celsius = 35
v_init = -70
			
global_ra=200.00 	// internal resistivity in ohm-cm 
Cm=1.5  		// specific membrane capacitance in uF/cm^2 
Cmy=0.075 		// capacitance in myelin 
Rm=40000		// specific membrane resistivity in ohm-cm^2  
Rn=50			// nodal resistivity 
Vleak=-66		// leak reversal -66 in Cs+
Vrest=-70		// resting potential -60 in control, -66 in Cs+

ttxScale = 0.5		// amount that 20 nM TTX scales the available Na conductance; 1=no block; 0 = complete block

spinelimit=100      	// distance beyond which to modify for spines 
spinefactor=2.0     	// factor by which to change passive properties 

gnainit0 = 0.042	// Na conductance at soma
gnaslope0 = 0.000025	// Na channel density decay per um
gnabar=0.042		// sodium conductance 
gnode=0 //40.0		// sodium conductance at a node; MSC switched this 

setgk = .036		// A-type potassium starting density, used in init_bday.hoc
setokslope = 0		// slope of A-type potassium conductance along individual oblique branches. set to 0 in all simulations

gcad = 0.00125		// L-type Ca density, from Poirazi et al., 2003
caslope = 0

gkdr=0.040          	// delayed rectifier density 
gkap=setgk          	// proximal A-type potassium starting density 
gkad=setgk          	// distal A-type potassium  starting density 

dlimit=300          	// cut-off for increase of A-type density 
dprox=50           	// distance to switch from proximal to distal type 
dslope=0.01         	// slope of A-type density 

okslope = setokslope	// oblique potassium channel gradient 
okmax = .5		// max potassium channel conductance  

ampaWeight = 0.00018 	// in uS; Jarsky et al., 2005
nmdaWeight = 0.00018	// in uS

theSeed = 1		// seed of random number generator

numSyn = 150	 	// number of synapses

slowInact = 0		// amount of slow inactivation.  1 = no slow inact; 0 = complete slow inact

// gnaTuft0 and gnaTuftS are not used
gnaTuft0 = 0.04		// initial VGNaC denisty in the tuft
gnaTuftS = 0.00002	// slope of VGNaC density in the tuft

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