Modeling of glutamate-induced dynamical patterns.
Based on established physiological mechanisms, the paper presents a detailed computer model, which supports the hypothesis that temporal lobe epilepsy may be caused by failure of glutamate reuptake from the extracellular space. The elevated glutamate concentration causes an increased activation of NMDA receptors in pyramidal neurons, which in turn leads to neuronal dynamics that is qualitatively identical to epileptiform activity. We identify by chaos analysis a surprising possibility that muscarinergic receptors can help the system out of a chaotic regime.
Bentzen
N C K
NC
Department of Physics, The Technical University of Denmark, Fysikvej 309, 2800 Lyngby, Denmark. neuro@krefeld.dk
Zhabotinsky
A M
AM
Laugesen
J L
JL
D000200:Action Potentials / Q000502:physiology; D000818:Animals; D003198:Computer Simulation; D004833:Epilepsy, Temporal Lobe / Q000378:metabolism* / Q000503:physiopathology; D005110:Extracellular Space / Q000378:metabolism; D050491:Glutamate Plasma Membrane Transport Proteins / Q000378:metabolism; D018698:Glutamic Acid / Q000378:metabolism*; D006624:Hippocampus / Q000378:metabolism* / Q000503:physiopathology; D006801:Humans; D055641:Mathematical Concepts; D009434:Neural Pathways / Q000378:metabolism / Q000503:physiopathology; D017711:Nonlinear Dynamics; D017966:Pyramidal Cells / Q000378:metabolism*; D051381:Rats; D016194:Receptors, N-Methyl-D-Aspartate / Q000378:metabolism*; D013569:Synapses / Q000378:metabolism*; D009435:Synaptic Transmission / Q000502:physiology
D050491:Glutamate Plasma Membrane Transport Proteins; D016194:Receptors, N-Methyl-D-Aspartate; D018698:Glutamic Acid