Inhibition and glial-K+ interaction leads to diverse seizure transition modes (Ho & Truccolo 2016)

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Accession:190306
"How focal seizures initiate and evolve in human neocortex remains a fundamental problem in neuroscience. Here, we use biophysical neuronal network models of neocortical patches to study how the interaction between inhibition and extracellular potassium ([K+]o) dynamics may contribute to different types of focal seizures. Three main types of propagated focal seizures observed in recent intracortical microelectrode recordings in humans were modelled ..."
Reference:
1 . Ho ECY, Truccolo W (2016) Interaction between Synaptic Inhibition and Glial-Potassium Dynamics leads to Diverse Seizure Transition Modes in Biophysical Models of Human Focal Seizures J Comput Neurosci
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Model Information (Click on a link to find other models with that property)
Model Type: Realistic Network;
Brain Region(s)/Organism: Neocortex;
Cell Type(s): Abstract single compartment conductance based cell;
Channel(s): I K,Ca; I Sodium; I_AHP; I Potassium; I Calcium;
Gap Junctions:
Receptor(s): GabaA; Glutamate;
Gene(s):
Transmitter(s): Gaba; Glutamate;
Simulation Environment: C or C++ program;
Model Concept(s): Bursting; Delay; Epilepsy; Ion Channel Kinetics; Potassium buffering; Gamma oscillations;
Implementer(s): Ho, E [ernest_ho at brown.edu];
Search NeuronDB for information about:  GabaA; Glutamate; I K,Ca; I Sodium; I Calcium; I Potassium; I_AHP; Gaba; Glutamate;
 
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