Abstract
There is convincing evidence that excitatory amino acids, particularly glutamate (GLU) and aspartate (ASP), are involved in basic mechanism of epilepsy (for reviews see refs. 1,2,26). Thus, enhanced release, and reduced tissue levels, of excitatory amino acids have been reported in various animal models of epilepsy (9,13,20,24,34,41,44). Reduced levels of both GLU and ASP have also been demonstrated in tissue excised from human epileptic foci (42,43). In addition, excitatory amino acid antagonists have been shown to block epileptic seizures and epileptiform activity in both rodent and primate models of epilepsy (4,5,6,26,34,39,40).
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Mori, N., Wada, J.A. (1990). Does Electrical and Excitatory Amino Acid Kindling Share a Common Neurobiological Mechanism?. In: Wada, J.A. (eds) Kindling 4. Advances in Behavioral Biology, vol 37. Springer, Boston, MA. https://doi.org/10.1007/978-1-4684-5796-4_16
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DOI: https://doi.org/10.1007/978-1-4684-5796-4_16
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