Titlebook: Kindling 4; Juhn A. Wada Book 1990 Plenum Press, New York 1990 Aspartat.adenosine.amino acid.anatomy.brain.brainstem.cortex.development.el

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Genetic Contributions to Kindling: An Experimental Approach, populations through selective breeding, along with the reported variations in kindling rates among inbred strains of mice strongly suggests the contribution of genetics to kindling [2,6,17,18]. The rapid kindling rates of genetically epilepsy prone rats [29] and El mice [13] in comparison with appr

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Noradrenaline and Kindling Revisited,reatments that interfere with the actions of noradrenaline (NA). This body of research has given rise to the hypothesis that part of the mechanism of kindling may be a decrease in the effects of NA, produced either by a progressive suppression of the presynaptic release of NA. or a decline in the po

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The Kindling Process and Vulnerability to Status Epilepticus,pon a background of epileptogenesis resulting from amygdala kindling (1). We were initially interested in using the model to study the mechanisms by which the sustained seizures were initiated and maintained. However, we were struck by the extensive bilateral neuropathology resulting from a relative

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Frequency- and Time-Domain EEG Topographic Analysis of the Amygdala Kindling Evolution in the Cat,o evaluate. A great number of kindling experiments are performed in the rat, recording only the amygdaline or hippocampal ADs, with few if any, cortical recordings (a notorious exception are the works of Wada and his associates in sub-human primates), and correlating the ADs’ duration (rarely the fr

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Does Electrical and Excitatory Amino Acid Kindling Share a Common Neurobiological Mechanism?,y (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

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Involvement of Excitatory Amino Acids in the Mechanisms of Kindling, 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). Further

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Effect of Selective Lesions within the Substantia Nigra on the Anticonvulsant Effect of Antiepilepte propagation (1,2). Autoradiographic studies of 2-deoxyglucose metabolism have shown that activation of the SN is a stable feature of fully generalized convulsions induced by chemoconvulsants (3) or amygdala-kindling (4). Extracellular, single-cell recording studies have shown that SN neurons exhib