Glutamate and epilepsy

Epileptic syndromes have very diverse primary causes, which may be genetic, developmental or acquired. In rodent models, altering glutamate receptor or glutamate transporter expression by knockout or knockdown procedures can induce or suppress epileptic seizures. Regardless of the primary cause, syn...

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Bibliographic Details
Published in:	The Journal of nutrition Vol. 130; no. 4S Suppl; p. 1043S
Main Author:	Chapman, A G
Format:	Journal Article
Language:	English
Published:	United States 01-04-2000
Subjects:	Amino Acid Transport System X-AG Animals ATP-Binding Cassette Transporters - metabolism Epilepsy - physiopathology Glutamic Acid - physiology Humans Receptors, Glutamate - physiology Receptors, Metabotropic Glutamate - physiology
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Summary:	Epileptic syndromes have very diverse primary causes, which may be genetic, developmental or acquired. In rodent models, altering glutamate receptor or glutamate transporter expression by knockout or knockdown procedures can induce or suppress epileptic seizures. Regardless of the primary cause, synaptically released glutamate acting on ionotropic and metabotropic receptors appears to play a major role in the initiation and spread of seizure activity. In rodent models of acquired epilepsy and in human temporal lobe epilepsy, there is evidence for enhanced functional efficacy of ionotropic N-methyl-D-aspartate (NMDA) and metabotropic (Group I) receptors. In animal models of epilepsy, antagonists acting at NMDA receptors or at Group I metabotropic receptors have potent anticonvulsant actions.
ISSN:	0022-3166
DOI:	10.1093/jn/130.4.1043S