Synaptic plasticity in kindling.
Kindling is an experimental model of epilepsy resulting from progressive activity-dependent changes in neuronal structure and function. During kindling, pathologic changes occur at various levels of organization of the nervous system, ranging from altered gene-expression in individual neurons to the loss of specific neuronal populations and the rearrangement of synaptic connections. This chapter summarizes recent findings about the long-lasting (plastic) nature of the alterations at the level of single neurons with emphasis on the role of altered excitatory and inhibitory amino acid receptors. The modified synaptic ligand-gated ion channels (i.e., "epileptic receptors") may ultimately be responsible for the kindling epileptogenesis.
Mody
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Department of Neurology, University of California, School of Medicine, Los Angeles 90095-1769, USA.
D000818:Animals; D006801:Humans; D007473:Ion Channels / Q000502:physiology; D007696:Kindling, Neurologic / Q000502:physiology*; D009473:Neuronal Plasticity / Q000502:physiology*; D011963:Receptors, GABA-A / Q000502:physiology; D016194:Receptors, N-Methyl-D-Aspartate / Q000378:metabolism; D013569:Synapses / Q000378:metabolism / Q000502:physiology*
D007473:Ion Channels; D011963:Receptors, GABA-A; D016194:Receptors, N-Methyl-D-Aspartate