Febrile seizure-induced modifications to Ih (Chen et al 2001)

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Modeling and experiments in the paper Chen K,Aradi I, Thom N,Eghbal-Ahmadi M, Baram TZ, and Soltesz I (2001) support the hypothesis that modified Ih currents strongly influence inhibitory inputs in CA1 cells and that the depolarizing shift in Ih activation plays a primary role in this process. Please see the paper for details. Some modeling details are available at http://www.ucihs.uci.edu/anatomy/soltesz/supp.htm Correspondance should be addressed to isoltesz@uci.edu (modeling was done by Ildiko Aradi, iaradi@uci.edu)
1 . Chen K, Aradi I, Thon N, Eghbal-Ahmadi M, Baram TZ, Soltesz I (2001) Persistently modified h-channels after complex febrile seizures convert the seizure-induced enhancement of inhibition to hyperexcitability. Nat Med 7:331-7 [PubMed]
Model Information (Click on a link to find other models with that property)
Model Type: Channel/Receptor;
Brain Region(s)/Organism:
Cell Type(s): Hippocampus CA1 pyramidal GLU cell;
Channel(s): I Na,t; I K; I h;
Gap Junctions:
Simulation Environment: NEURON;
Model Concept(s): Action Potential Initiation; Activity Patterns; Bursting; Ion Channel Kinetics; Action Potentials; Epilepsy; Rebound firing;
Implementer(s): Aradi, Ildiko [IAradi at uci.edu];
Search NeuronDB for information about:  Hippocampus CA1 pyramidal GLU cell; I Na,t; I K; I h;


proc HT() {

	cell = new HTCell()
	print "HT treated cell with rebound firing"
	access cell.soma

proc Control() {

	cell = new Cell()
	print "Control (sham treated) cell with no rebound firing"
	access cell.soma

xpanel("Figure 5B",1)
xlabel("Press a button to plot")
xbutton(" HT ","HT()")
xlabel(" rebound firing ")
xbutton(" Control ","Control()")
xlabel(" cell no rebound firing")

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