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Titlebook: Generalized Non-Convulsive Epilepsy: Focus on GABA-B Receptors; C. Marescaux,M. Vergnes,R. Bernasconi Conference proceedings 1992 Springer

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Conference proceedings 1992is supplementum will also provide very recent information on putative mechanisms underlying generalized absence seizures. Third, various experimental approaches aimed at investigating the neural substrate of this particular kind of epilepsy are described with various electrophysiological, pharmacolo
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Conference proceedings 1992ological and genetic characteristics differ from those of convulsive or focal epilepsies. No underlying structural or biochemical abnormality has been identified for generalized absence seizures and the etiology of this disorder is unknown. It is unlikely that the precise pathophysiology of GNCE can
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acerbated by GABAergic agonists, a property unique to experimental absence seizures. These models are predictable, reproducible, and easy to standardize. They are useful both in studying mechanisms of pathogenesis of absence seizures as well as in screening for antiabsence activity of potential antiepileptic drugs.
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Pharmacological models of generalized absence seizures in rodents,acerbated by GABAergic agonists, a property unique to experimental absence seizures. These models are predictable, reproducible, and easy to standardize. They are useful both in studying mechanisms of pathogenesis of absence seizures as well as in screening for antiabsence activity of potential antiepileptic drugs.
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Discrete Data Fourier Deconvolution,relay and reticular nuclei, definitely suppressed ipsilateral SWD, and pentylenetetrazol, THIP or gammabutyrolactone failed to restore the cortical SWD..These results demonstrate that the neocortex and the specific thalamic nuclei are both necessarily involved in the generation of SWD in absence epilepsy.
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An Iconic Theory of Criminal Justice,ved Cd. injection into the ventroposterior complex (VP) showed only small changes in ipsilateral SW. It is concluded that Ca.-dependent oscillatory properties of the RTN are critical for the expression of genetically determined SW discharges in the Wistar model.
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