Literature DB >> 10873292

'Non-synaptic' mechanisms in seizures and epileptogenesis.

F E Dudek1, T Yasumura, J E Rash.   

Abstract

The role of 'non-synaptic' mechanisms (i.e. those mechanisms that are independent of active chemical synpases) in the synchronization of neuronal activity during seizures and their possible contribution to chronic epileptogenesis are summarized. These 'non-synaptic' mechanisms include electrotonic coupling through gap junctions, electrical field effects (i.e. ephaptic transmission), and ionic interactions (e.g. increases in the extracellular concentration of K(+)). Several lines of evidence indicate that granule cells and pyramidal cells of the hippocampus, and probably other cortical neurons, can generate synchronized electrical activity after active chemical synaptic transmission has been blocked. This synchronized activity is sensitive to alterations in the size of the extracellular space, thus suggesting that electrical field effects and ionic mechanisms contribute to this synchronized activity. Recent studies also indicate that 'non-synaptic' synchronization is quite prominent early in development. Electrophysiological data from hippocampal and neocortical slices have led to a re-interpretation of the fast prepotentials (i.e. partial spikes) recorded in cortical pyramidal cells, suggesting that they may not be due to dendritic spike generation. Improvement in freeze-fracture ultrastructural techniques have led to a re-assessment of previous data on gap junctions in the nervous system and opened new approaches to the quantitative analysis and characterization of gap junctions on glia and neurons. Finally, new methods of dye/tracer coupling have the potential to provide a more rigorous basis for evaluating gap junctions and electrotonic communication between neurons in the mammalian central nervous system. Therefore, recent data continue to suggest that gap junctions and electrotonic coupling play an important role in neural integration, although additional studies using new techniques will be needed to address some of the controversial issues that have arisen over the last several decades. Copyright 1998 Academic Press.

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Year:  1998        PMID: 10873292     DOI: 10.1006/cbir.1999.0397

Source DB:  PubMed          Journal:  Cell Biol Int        ISSN: 1065-6995            Impact factor:   3.612


  31 in total

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2.  Calcium-Sensitive Translocation of Calmodulin and Neurogranin between Soma and Dendrites of Mouse Hippocampal CA1 Neurons.

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4.  An organotypic hippocampal slice culture model of excitotoxic injury induced spontaneous recurrent epileptiform discharges.

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6.  Characteristics of intercellular contacts in the reticular nucleus of the thalamus in WAG/Rij rats.

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7.  Role of paroxysmal depolarization in focal seizure activity.

Authors:  Andrew K Tryba; Edward M Merricks; Somin Lee; Tuan Pham; SungJun Cho; Douglas R Nordli; Tahra L Eissa; Robert R Goodman; Guy M McKhann; Ronald G Emerson; Catherine A Schevon; Wim van Drongelen
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Review 8.  Physiological bases of the K+ and the glutamate/GABA hypotheses of epilepsy.

Authors:  Mauro DiNuzzo; Silvia Mangia; Bruno Maraviglia; Federico Giove
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Review 9.  Mechanisms of intrinsic epileptogenesis in human gelastic seizures with hypothalamic hamartoma.

Authors:  Jie Wu; Ming Gao; Jian-Xin Shen; Shen-Feng Qiu; John F Kerrigan
Journal:  CNS Neurosci Ther       Date:  2014-12-12       Impact factor: 5.243

10.  Field effects in the CNS play functional roles.

Authors:  Shennan A Weiss; Donald S Faber
Journal:  Front Neural Circuits       Date:  2010-05-18       Impact factor: 3.492

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