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

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Accession:116769
This model was set up to dissect the relative contribution of different channels to the spine calcium transients measured at single spines.
Reference:
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]
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;
Gene(s):
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; 
load_file("nrngui.hoc")

/********************************************************************
load cell morphology                           
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xopen("cellmorphology.hoc")


/********************************************************************
load spinehead, spineneck                      
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xopen("spine.hoc")


/********************************************************************
set up section lists and initialize parameters 
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xopen("iniparameter.hoc")


/********************************************************************
load figure                            
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load_file("fig4.hoc")

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