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Contribution of ATP-sensitive potassium channels in the neuronal network (Huang et al. 2009)
Accession: 120243
Epileptic seizures in diabetic hyperglycemia (DH) are not uncommon. This study aimed to determine the acute behavioral, pathological, and electrophysiological effects of status epilepticus (SE) on diabetic animals. ... We also used a simulation model to evaluate intracellular adenosine triphosphate (ATP) and neuroexcitability. ... In the simulation, increased intracellular ATP concentration promoted action potential firing. This finding that rats with DH had more brain damage after SE than rats without diabetes suggests the importance of intensively treating hyperglycemia and seizures in diabetic patients with epilepsy.
Reference: Huang CW, Cheng JT, Tsai JJ, Wu SN, Huang CC (2009) Diabetic Hyperglycemia Aggravates Seizures and Status Epilepticus-induced Hippocampal Damage. Neurotox Res 15:71-81 [PubMed]
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Model Information (Click on a link to find other models with that property)
Model Type:  Network;
Brain Region(s)/Organism:  
Cell Type(s):   Hodgkin-Huxley neuron;
Channel(s):  ATP-senstive potassium current;  
Gap Junctions:  
Receptor(s):  
Gene(s):  
Transmitter(s):  
Simulation Environment:  XPP;
Model Concept(s):  Action Potentials; Epilepsy;
Implementer(s):  Wu, Sheng-Nan [snwu at mail.ncku.edu.tw];
Search NeuronDB for information about:  ATP-senstive potassium current;
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Network-Katp
readme.html
Figure6A.JPG
hh200x50_Katp.ode
                            
This is the readme.txt for the models associated with the paper

Huang CW, Cheng JT, Tsai JJ, Wu SN, Huang CC. Diabetic hyperglycemia 
aggravates seizures and status epilepticus-induced hippocampal damage. 
Neurotox Res (2009) 15:71-81.

Abstract:

Epileptic seizures in diabetic hyperglycemia (DH) are not
uncommon. This study aimed to determine the acute behavioral,
pathological, and electrophysiological effects of status epilepticus
(SE) on diabetic animals. Adult male Sprague-Dawley rats were first
divided into groups with and without streptozotocin (STZ)-induced
diabetes, and then into treatment groups given a normal saline (NS)
(STZ-only and NS-only) or a lithium-pilocarpine injection to induce
status epilepticus (STZ + SE and NS + SE). Seizure susceptibility,
severity, and mortality were evaluated. Serial Morris water maze test
and hippocampal histopathology results were examined before and 24 h
after SE. Tetanic stimulation-induced long-term potentiation (LTP) in
a hippocampal slice was recorded in a multi-electrode dish system. We
also used a simulation model to evaluate intracellular adenosine
triphosphate (ATP) and neuroexcitability. The STZ + SE group had a
significantly higher percentage of severe seizures and SE-related
death and worse learning and memory performances than the other three
groups 24 h after SE. The STZ + SE group, and then the NS + SE group,
showed the most severe neuronal loss and mossy fiber sprouting in the
hippocampal CA3 area. In addition, LTP was markedly attenuated in the
STZ + SE group, and then the NS + SE group. In the simulation,
increased intracellular ATP concentration promoted action potential
firing. This finding that rats with DH had more brain damage after SE
than rats without diabetes suggests the importance of intensively
treating hyperglycemia and seizures in diabetic patients with
epilepsy.

--------------------------

To run the model:
XPP: start with the command
xpp ode\hh200x50_Katp.ode
(or xppaut hh200x50_Katp.ode)

Mouse click on Xi vs t, and change to VE30
then, click on Initialconds, and then (G)o.
This makes a trace similar to fig 6A  in the paper of Huang et al. 

Figure 6A

Mouse click Viewaxes, and Array.  After appropriate changes, a figure
similar to Fig 6B should appear.

Bard Ermentrout's website http://www.pitt.edu/~phase/
describes how to get and use xpp (Bard wrote xpp).

The model file was submitted by:
Dr. Sheng-Nan Wu
Department of Physiology
Natl Cheng Kung U Med Coll
Tainan 70101, Taiwan

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