Synaptic plasticity in kindling.

I Mody

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PubMed · 10514851

Synaptic plasticity in kindling.

I Mody

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Abstract

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.

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Animals Humans Ion Channels Kindling, Neurologic Neuronal Plasticity Receptors, GABA-A Receptors, N-Methyl-D-Aspartate Synapses Journal Article Research Support, Non-U.S. Gov't Research Support, U.S. Gov't, P.H.S.Review

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I Mody. 1999. Synaptic plasticity in kindling.. https://pubmed.ncbi.nlm.nih.gov/10514851/

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