Abstract
There are several lines of evidence that excitatory amino acids (EAA) receptors, which have a rather ubiquitous distribution in the CNS play a role in the genesis of epilepsy. Systemic or intracerebroventricular injections of EAA agonists (glutamate, NMDA, kainate, quisqualate) were all demonstrated to induce epilepsy (22), while their antagonists were potent antiepileptic or anticonvulsant agents in a wide variety of animal models (5,6). Furthermore, epileptic activities were often associated with an increase in the release of the putative endogenous transmitters aspartate and glutamate (7,15,29). There exist at least three different subclasses of EAA receptors (NMDA, quisqualate and kainate) and these multiple receptors may lead different responses to the same transmitter (8). In addition, it appears that ions are able to modulate their activation (18). Among these subclasses, most of the studies focused, in part because of the relative abundance of NMDA-antagonists, on the role of the NMDA-receptor which is mainly involved in the plasticity of the central nervous system and the generation of oscillatory activity (38). Several results indicate that it plays too a crucial role in epilepsy.
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© 1990 Plenum Press, New York
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Rondouin, G., Lerner-Natoli, M., Chicheportiche, R., Kamenka, JM. (1990). Involvement of Excitatory Amino Acids in the Mechanisms of Kindling. 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_17
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DOI: https://doi.org/10.1007/978-1-4684-5796-4_17
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