Spine neck plasticity controls postsynaptic calcium signals (Grunditz et al. 2008)

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This model was set up to dissect the relative contribution of different channels to the spine calcium transients measured at single spines.
1 . Grunditz A, Holbro N, Tian L, Zuo Y, Oertner TG (2008) Spine neck plasticity controls postsynaptic calcium signals through electrical compartmentalization. J Neurosci 28:13457-66 [PubMed]
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Model Information (Click on a link to find other models with that property)
Model Type: Synapse;
Brain Region(s)/Organism:
Cell Type(s): Hippocampus CA1 pyramidal GLU cell;
Channel(s): I Calcium; I R;
Gap Junctions:
Receptor(s): AMPA; NMDA;
Transmitter(s): Glutamate;
Simulation Environment: NEURON;
Model Concept(s): Calcium dynamics;
Implementer(s): Mueller, Asa [asa.mueller at fmi.ch];
Search NeuronDB for information about:  Hippocampus CA1 pyramidal GLU cell; AMPA; NMDA; I Calcium; I R; Glutamate;
Create a spine with a spine neck 
connected to the parant dendrite dendA5_00

{create spine_neck}
{dendA5_00 connect spine_neck(0),0.8}
{access spine_neck}
necklength = 1  /*spine neck length in um*/
neckdiam = 0.0394 /*spine neck diameter*/
spine_neck {nseg = 2
            for j = 0, nseg-1 {
                ty = (j*necklength)/(nseg-1)

{create spine_head}
{spine_neck connect spine_head(0), 1}
{access spine_head}
spineradius = 0.297
spine_head {nseg = 7
            for i = 0, nseg-1 {
                ty = -(i*2*spineradius)/(nseg-1)
                td = 2*sqrt(spineradius^2-(ty+spineradius)^2)
                if (td<neckdiam){
                    td = neckdiam