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Kindling is an experimental model of epilepsy that involves activity-dependent changes in neuronal structure and function. During kindling, pathological changes may occur at several organizational levels of the nervous system, from alterations in gene-expression in individual neurons to the loss of specific neuronal populations and rearrangement of synaptic connectivity resulting from sustained stimulation of major excitatory pathways. This review summarizes recent developments in alterations at single neuronal and molecular levels that may be responsible for kindling epileptogenesis.
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István Módy (1993) studied this question.
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