HERG K+ channels spike-frequency adaptation (Chiesa et al 1997)

 Download zip file 
Help downloading and running models
Accession:57910
Spike frequency adaptation has contributions from the IHERG current (encoded by the human eag-related gene (HERG); Warmke & Ganetzky, 1994), which develops with slow kinetics during depolarization and contributes to the repolarization of the long action potentials typically present in the heart. IHERG is one of the delayed rectifier currents (IK(r)) of the heart, and HERG mutations are associated with one of the cardiac arrhythmia LQT syndromes (LQT2). See paper for more and details.
Reference:
1 . Chiesa N, Rosati B, Arcangeli A, Olivotto M, Wanke E (1997) A novel role for HERG K+ channels: spike-frequency adaptation. J Physiol 501 ( Pt 2):313-8 [PubMed]
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): Neuroblastoma;
Channel(s): I_HERG;
Gap Junctions:
Receptor(s):
Gene(s):
Transmitter(s):
Simulation Environment: XPPAUT;
Model Concept(s): Action Potentials; Long-QT; Spike Frequency Adaptation;
Implementer(s): Wu, Sheng-Nan [snwu at mail.ncku.edu.tw]; Chang, Han-Dong; Wu, Jiun-Shian [coolneon at gmail.com];
Search NeuronDB for information about:  I_HERG;
/
kir_sim
readme.txt
kir_sim.ode
samplerun.jpg
                            
This is the readme.txt for the model associated with the paper

Chiesa N, Rosati B, Arcangeli A, Olivotto M, Wanke E. A novel role 
for HERG K+ channels: spike-frequency adaptation. J Physiol 1997;501:313-318

Abstract:
1. The regular firing of a Hodgkin-Huxley neurone endowed with fast Na+ 
and delayed K+ channels can be converted into adapting firing by appending 
HERG (human eag-related gene) channels. 2. The computer model predictions 
were verified by studying the firing properties of F-11 DRG neurone x 
neuroblastoma hybrid cells induced to differentiate by long- term exposure 
to retinoic acid. These cells, which express HERG currents (IHERG), show 
clear spike-frequency adaptation of their firing when current clamped with 
long depolarizations. 3. In agreement with the prediction, the selective 
blocking of IHERG by class III antiarrhythmic drugs always led to the 
disappearance of the spike- frequency adaptation, and the conversion of 
adapting firing to regular firing. 4. It is proposed that, in addition to their 
role in the repolarization of the heart action potential, HERG channels may 
sustain a process of spike-frequency adaptation, and hence contribute to the 
control of burst duration in a way that is similar to that of the K+ currents, 
IAHP, IC and IM. In addition to the known cardiac arrhythmia syndrome 
(LQT2), genetic mutations or an altered HERG expression could lead to 
continuous hyperexcitable states sustained by the inability of nerve or endocrine 
cells to accommodate to repetitive stimuli. This might help in clarifying the 
pathogenesis of still undefined idiopathic familial epilepsies. 
---

To run the models:
XPP: start with the command

xpp ode\kir_sim.ode

Mouse click on Initialconds, and then (G)o.
This makes a trace similar to fig 1E of the paper.

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

These model files were submitted by:

Dr. Sheng-Nan Wu
Dept Physiol
Natl Cheng Kung U Med Coll
Tainan 70101, Taiwan

snwu@mail.ncku.edu.tw

Loading data, please wait...