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Synaptic plasticity in kindling.

¹Department of Neurology, University of California, School of Medicine, Los Angeles 90095-1769, USA.

Advances in Neurology

|October 9, 1999

Summary

Kindling, an epilepsy model, involves progressive neuronal changes. Altered amino acid receptors and "epileptic receptors" in neurons are key to developing kindling epileptogenesis.

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Area of Science:

Neuroscience
Epilepsy Research
Molecular Biology

Background:

Kindling is an experimental epilepsy model.
It involves progressive, activity-dependent neuronal changes.
Pathologic changes occur at multiple nervous system levels.

Purpose of the Study:

Summarize recent findings on long-lasting neuronal alterations in kindling.
Emphasize the role of altered amino acid receptors.
Investigate the contribution of modified synaptic ligand-gated ion channels to epileptogenesis.

Main Methods:

Review of recent scientific literature on kindling.
Analysis of studies focusing on neuronal plasticity.
Examination of research on excitatory and inhibitory amino acid receptors.

Main Results:

Kindling induces long-lasting plastic alterations in single neurons.
Changes involve altered gene expression, neuronal loss, and synaptic rearrangement.
Modified excitatory and inhibitory amino acid receptors are implicated.

Conclusions:

Altered amino acid receptors contribute significantly to kindling.
Modified synaptic ligand-gated ion channels, termed "epileptic receptors", are crucial.
These receptors are likely responsible for kindling epileptogenesis.

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