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The role of ATP-sensitive potassium channels in a hippocampal neuron (Huang et al. 2007)

modeldb.science/87762

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Name		Name	Last commit message	Last commit date
Latest commit History 1 Commit
JNS_Katp.pdf		JNS_Katp.pdf
NeuronKATP_Stoch.ode		NeuronKATP_Stoch.ode
Neuron_Figure.JPG		Neuron_Figure.JPG
readme.html		readme.html

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<html><pre>
This is the readme.txt for the model associated with the paper

Huang CW et al. Glucose and hippocampal neuronal excitability: 
role of ATP-sensitive potassium channel. J Neurosci Res 2007,
[Epub ahead of print]

Abstract:
Hyperglycemia-related neuronal excitability and epileptic seizures 
are not uncommon in clinical practice. However, their underlying 
mechanism remains elusive. ATP-sensitive K(+) (K(ATP)) channels are 
found in many excitable cells, including cardiac myocytes, 
pancreatic beta cells, and neurons. These channels provide a link 
between the electrical activity of cell membranes and cellular 
metabolism. We investigated the effects of higher extracellular 
glucose on hippocampal K(ATP) channel activities and neuronal 
excitability. The cell-attached patch-clamp configuration on 
cultured hippocampal cells and a novel multielectrode recording 
system on hippocampal slices were employed. In addition, a 
simulation modeling hippocampal CA3 pyramidal neurons (Pinsky-Rinzel 
model) was analyzed to investigate the role of K(ATP) channels in 
the firing of simulated action potentials. We found that incremental 
extracellular glucose could attenuate the activities of hippocampal 
K(ATP) channels. The effect was concentration dependent and involved 
mainly in open probabilities, not single-channel conductance. 
Additionally, higher levels of extracellular glucose could enhance 
neuropropagation; this could be attenuated by diazoxide, a K(ATP) 
channel agonist. In simulations, high levels of intracellular ATP, 
used to mimic increased extracellular glucose or reduced conductance 
of K(ATP) channels, enhanced the firing of action potentials in model 
neurons. The stochastic increases in intracellular ATP levels also 
demonstrated an irregular and clustered neuronal firing pattern. This 
phenomenon of K(ATP) channel attenuation could be one of the underlying 
mechanisms of glucose-related neuronal hyperexcitability and propagation.

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To run the models:
XPP: start with the command
xpp ode\NeuronKATP_Stoch.ode
select Initialconds -> Go
This simulation will make graphs similar to figure 6A in the paper
or Neuron_Figure.jpg:

<img src="Neuron_Figure.JPG" alt="Example run">

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

These model files were submitted by:

Drs. Sheng-Nan Wu and Ching-Wei Huang
National Cheng Kung University Medical Center
Tainan 70101, Taiwan
[email protected]