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CA1 pyramidal neuron synaptic integration (Bloss et al. 2016)

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Accession:187610
"... We examined synaptic connectivity between molecularly defined inhibitory interneurons and CA1 pyramidal cell dendrites using correlative light-electron microscopy and large-volume array tomography. We show that interneurons can be highly selective in their connectivity to specific dendritic branch types and, furthermore, exhibit precisely targeted connectivity to the origin or end of individual branches. Computational simulations indicate that the observed subcellular targeting enables control over the nonlinear integration of synaptic input or the initiation and backpropagation of action potentials in a branchselective manner. Our results demonstrate that connectivity between interneurons and pyramidal cell dendrites is more precise and spatially segregated than previously appreciated, which may be a critical determinant of how inhibition shapes dendritic computation."
Reference:
1 . Bloss EB, Cembrowski MS, Karsh B, Colonell J, Fetter RD, Spruston N (2016) Structured Dendritic Inhibition Supports Branch-Selective Integration in CA1 Pyramidal Cells. Neuron 89:1016-30 [PubMed]
Model Information (Click on a link to find other models with that property)
Model Type: Neuron or other electrically excitable cell;
Brain Region(s)/Organism:
Cell Type(s): Hippocampus CA1 pyramidal GLU cell;
Channel(s): I Na,t; I K;
Gap Junctions:
Receptor(s): AMPA; NMDA; Gaba;
Gene(s):
Transmitter(s):
Simulation Environment: NEURON;
Model Concept(s): Synaptic Integration;
Implementer(s): Cembrowski, Mark S [cembrowskim at janelia.hhmi.org];
Search NeuronDB for information about:  Hippocampus CA1 pyramidal GLU cell; AMPA; NMDA; Gaba; I Na,t; I K;
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arrayTomography
README.txt
dists.mod *
eff.mod *
exc.mod
id.mod *
inh.mod
kad.mod *
kap.mod *
kdr.mod *
na3.mod *
nmdaSyn.mod
syns.mod *
activateExcitation.hoc
activateInhibition.hoc
addChannels.hoc *
addExcitation.hoc
addVgatInhibition.hoc
channelParameters.hoc *
flagVgatInhibition.hoc
getBranchOrder.hoc *
idMorph.hoc
inhibitionBiophysics.hoc
initializationAndRun.hoc *
loadMorph.hoc *
mosinit.hoc *
naceaxon.nrn *
processMorph.hoc *
proofreadMorph.hoc *
resetNSeg.hoc *
start.hoc
synHelperScripts.hoc
twinApical.swc *
                            
celsius = 35
v_init=-70
global_ra=200.00 	// internal resistivity in ohm-cm 
Cm=1.5 //0.75		// 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=-46		// switched from -66, in order to give a proper resting potential
Vrest=-70		// resting potential -60 in control, -66 in Cs+

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

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

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; 0.00018 used in Jarsky et al 2005
nmdaWeight = 0.00018	// in uS

gnaSoma = 0.1
gnaSr = 0.03
gnaSlm = 0.03

// Inhibition parameters.
inhRev = -75

npyTau1 = 0.1
npyTau2 = 10
sstTau1 = 0.2 // from Maccaferri et al., 2000
sstTau2 = 18 // from Maccaferri et al., 2000
npyWeight = 0.001 // from Maccaferri et al., 2000
sstWeight = 0.001 // from Maccaferri et al 2000

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