ContentsI. Introduction 739 A. General Background 739 B. Free Radicals and Single Electron Oxidations 742 C. A Cellular Model 742 D. Peroxidase Oscillator Phenomenology 743 II. Biochemical Model 743 A. Nonenzymatic Oxygen Radical Reactions 745 B. Preliminary Reactions 745 C. Principal Reactions 746 D. Compound III Reactions 747 E. Reactions of NAD • and OH • 747 F. Role of Methylene Blue 748 G. Role of 2,4-Dichlorophenol 748 III. Abstract Models 749 IV. Chemically Realistic Models 749 V. Critical Comments and Connection between Models and Experiments 751 A. Critique of Experiments 751 B. Critique of Theories 753 VI. Future Directions 753 VII. Appendix. Useful Constants for Characterizing Reactants Involved in the Peroxidase−Oxidase Reaction 754 VIII. Acknowledgments 754 IX. References 754

A coupled ordinary differential equation lattice model for the CA3 region of the hippocampus (a common location of the epileptic focus) is developed. This model consists of a hexagonal lattice of nodes, each describing a subnetwork consisting of a group of prototypical excitatory pyramidal cells and a group of prototypical inhibitory interneurons connected via on/off excitatory and inhibitory synapses. The nodes communicate using simple rules to simulate the diffusion of extracellular potassium. Both the integration time over which a node's trajectory is integrated before the diffusional event is allowed to occur and the level of inhibition in each node were found to be important parameters. Shorter integration times lead to total synchronization of the lattice (similar to synchronous neural activity occurring during a seizure) whereas longer times cause more random spatiotemporal behavior. Moderately diminished levels of inhibition lead to simple nodal oscillatory behavior. It is postulated that both the lack of inhibition and an alteration in conduction time may be necessary for the development of a behaviorally manifest seizure. (c) 1999 American Institute of Physics.

No abstract

No abstract

No abstract