ModelDB: Effect of slowly inactivating IKdr to delayed firing of action potentials (Wu et al. 2008)

Effect of slowly inactivating IKdr to delayed firing of action potentials (Wu et al. 2008)

Accession: 114108

"The properties of slowly inactivating delayed-rectifier K+ current (IKdr) were investigated in NG108-15 neuronal cells differentiated with long-term exposure to dibutyryl cyclic AMP. ... The computer model, in which state-dependent inactivation of IKdr was incorporated, was also implemented to predict the firing behavior present in NG108-15 cells. ... Our theoretical work and the experimental results led us to propose a pivotal role of slowly inactivating IKdr in delayed firing of APs in NG108-15 cells. The results also suggest that aconitine modulation of IKdr gating is an important molecular mechanism through which it can contribute to neuronal firing."
Reference: Wu SN, Chen BS, Lin MW, Liu YC (2008) Contribution of slowly inactivating potassium current to delayed firing of action potentials in NG108-15 neuronal cells: experimental and theoretical studies. J Theor Biol 252:711-21 [PubMed]

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Model Information (Click on a link to find other models with that property)

Model Type:	Neuron or other electrically excitable cell; Channel;
Brain Region(s)/Organism:
Cell Type(s):	Neuroblastoma; NG108-15 neuronal cell;
Channel(s):	I Na,t; I K; I Sodium; I Potassium;
Gap Junctions:
Receptor(s):
Gene(s):
Transmitter(s):
Simulation Environment:	XPP;
Model Concept(s):	Activity Patterns; Action Potentials; Delay;
Implementer(s):	Wu, Sheng-Nan [snwu at mail.ncku.edu.tw]; Chen, Bing-Shuo;

Search NeuronDB for information about: I Na,t; I K; I Sodium; I Potassium;

Model files

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This is the readme.txt for the models associated with the paper

Wu SN, Chen BS, Lin MW, Liu YC. Contribution of slowly inactivating potassium
current to delayed firing of action potentials in NG108-15 neuronal cells:
Experimental and theoretical studies. J Theor Biol 2008;252:711-21

Abstract:

The properties of slowly inactivating delayed-rectifier K+ current
(IKdr) were investigated in NG108-15 neuronal cells differentiated
with long-term exposure to dibutyryl cyclic AMP. Slowly inactivating
IKdr could be elicited by prolonged depolarizations from -50 to +50
mV. These outward K+ currents were found to decay at potentials above
-20 mV, and the decay became faster with greater depolarization. Cell
exposure to aconitine resulted in the reduction of IKdr amplitude
along with an accelerated decay of current inactivation. Under
current-clamp recordings, a delay in the initiation of action
potentials (APs) in response to prolonged current stimuli was observed
in these cells.  Application of aconitine shortened the AP initiation
in combination with an increase in both width of spike discharge and
firing frequency. The computer model, in which state-dependent
inactivation of IKdr was incorporated, was also implemented to predict
the firing behavior present in NG108-15 cells. As the inactivation
rate constant of IKdr was elevated, the firing frequency was
progressively increased along with a shortening of the latency for AP
appearance. Our theoretical work and the experimental results led us
to propose a pivotal role of slowly inactivating IKdr in delayed
firing of APs in NG108-15 cells. The results also suggest that
aconitine modulation of IKdr gating is an important molecular
mechanism through which it can contribute to neuronal firing.

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

To run the model:
XPP: start with the command
xppaut JTBfig07.ode

Mouse click on Initialconds, and then (G)o.

This makes a trace similar to fig 6 or 7a in the paper of Wu et
al. 2008:




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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