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Rejuvenation model of dopamine neuron (Chan et al. 2007)
Accession: 97860
Model files for the paper C. Savio Chan, et al. 'Rejuvenation' protects neurons in mouse models of Parkinson's disease, Nature 447, 1081-1086(28 June 2007).
Reference: Chan CS, Guzman JN, Ilijic E, Mercer JN, Rick C, Tkatch T, Meredith GE, Surmeier DJ (2007) 'Rejuvenation' protects neurons in mouse models of Parkinson's disease. Nature 447:1081-6 [PubMed]
Citations  Citation Browser
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):   
Channel(s):  I Na,t; I K; I h; I K,Ca; I Sodium; I Calcium; I Potassium;  
Gap Junctions:  
Receptor(s):  
Gene(s):  Cav1.3 CACNA1D;
Transmitter(s):  
Simulation Environment:  Neuron;
Model Concept(s):  Simplified Models; Action Potentials; Parkinson's;
Implementer(s):  Held, Joshua [j-held at northwestern.edu];
Search NeuronDB for information about:  I Na,t; I K; I h; I K,Ca; I Sodium; I Calcium; I Potassium;
Model files   Download zip file   Auto-launch             Help downloading and running models      Versions
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rejuvenation
mod
readme.html
S5a.jpg
init.hoc
mosinit.hoc
panels.hoc
build.hoc
graph.hoc
                            
NEURON mod files from the paper:

C. Savio Chan, Jaime N. Guzman, Ema Ilijic, Jeff N. Mercer, Caroline
Rick, Tatiana Tkatch, Gloria E. Meredith & D. James Surmeier
'Rejuvenation' protects neurons in mouse models of Parkinson's
disease, Nature 447, 1081-1086(28 June 2007)



This is the model demonstrated in Supplementary Information:

Figure S5: Computer simulation of the role of HCN gating in pacemaking
of DA neurons. a. NEURON simulation of autonomous spiking in an SNc DA
neuron.  Elimination of voltage-dependent Na+ channels revealed Cav1.3
L-type Ca2+ channel dependent pacemaker potentials, similar to that
found in recorded neurons. b. Elevating intracellular cAMP in the
model following the model of Siegelbaum et al. 48 produced a rightward
shift in the voltage of activation for HCN channels. This shift
increased HCN currents in a simulated voltage clamp experiment in much
the same way as seen experimentally (see Supplementary Figs. 3,
4). c. Elimination of Cav1.3 L-type Ca2+ channel silenced pacemaking
activity in the model SNc DA neuron, resembling experimental
observation.  Elevating cAMP levels and shifting HCN voltage
dependence restored pacemaking activity in the face of Cav1.3 L-type
Ca2+ channel blockade.

Sample model usage:

Start the model with auto-launch in ModelDB or download and extract
the archive and then

under mswin:
------------
1) compile the mod files with mknrndll (in the mod directory)
2) double click on the mosinit.hoc file

under linux/unix:
-----------------
1) compile the mod files with nrnivmodl (in the mod directory)
2) start with "nrngui mosinit.hoc" in the rejuvenation directory


Once the simulation is started:
-------------------------------
1) Click Init & Run

2) Click the box to turn off Na channels to see the Cav1.3 L-type Ca2+
channel dependent pacemaker potentials

If all goes well you will create a figure similar to figure S5A in the
paper:

S5a figure

Questions on how to use this model can be directed to Josh Held,
j-held@northwestern.edu

20120112 kv4hh.mod solve method updated to cnexp from euler as per
http://www.neuron.yale.edu/phpbb/viewtopic.php?f=28&t=592

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