1995Psychiatry and Clinical NeurosciencesRequires access

Analyses of the molecular basis of kindling development

James O McNamara

Open publisher page 35 citations

Abstract

Kindling has become the most widely studied animal model of limbic epilepsy. Understanding the molecular basis of kindling development may provide novel therapeutic approaches to prevention of limbic epileptogenesis. I briefly describe the kindling model and outline the basis for my thinking that kindling represents a synaptic reorganization triggered by pathologic activity in the mature nervous system. The pathologic activity is postulated to evoke a cascade of gene expression driven, at least in part, by glutamate receptor activation. Evidence in support of this hypothesis is presented, as are future challenges that permit critical tests of these ideas.

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What this paper is about

Kindling has become the most widely studied animal model of limbic epilepsy. Understanding the molecular basis of kindling development may provide novel therapeutic approaches to prevention of limbic epileptogenesis. I briefly describe the kindling model and outline the basis for my thinking that kindling represents a synaptic reorganization triggered by pathologic activity in the mature nervous system. The pathologic activity is postulated to evoke a cascade of gene expression driven, at least in part, by glutamate receptor activation. Evidence in support of this hypothesis is presented, as are future challenges that permit critical tests of these ideas.

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Available abstract

Kindling has become the most widely studied animal model of limbic epilepsy. Understanding the molecular basis of kindling development may provide novel therapeutic approaches to prevention of limbic epileptogenesis. I briefly describe the kindling model and outline the basis for my thinking that kindling represents a synaptic reorganization triggered by pathologic activity in the mature nervous system. The pathologic activity is postulated to evoke a cascade of gene expression driven, at least in part, by glutamate receptor activation. Evidence in support of this hypothesis is presented, as are future challenges that permit critical tests of these ideas.

Key concepts: Kindling, Epileptogenesis, Neuroscience, Kindling model, Epilepsy, Psychology, Limbic system, Glutamate receptor

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