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ISBN:3211823409
Author: C. Marescaux,M. Vergnes,R. Bernasconi
ISBN13: 978-3211823408
Title: Generalized Non-Convulsive Epilepsy: Focus on GABA-B Receptors (Journal of Neural Transmission. Supplementa)
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Language: English
Category: Medicine
Publisher: Springer; 1 edition (August 11, 1992)
Pages: 200

Generalized Non-Convulsive Epilepsy: Focus on GABA-B Receptors (Journal of Neural Transmission. Supplementa) by C. Marescaux,M. Vergnes,R. Bernasconi



Generalized non convulsive epilepsy (GNCE), also called absence or petit mal epilepsy, is a disease appearing during childhood. EEG, clinical, pharmacological and genetic characteristics differ from those of convulsive or focal epilepsies. It is unlikely that the precise pathophysiology of GNCE can be resolved in studies that focus on humans. Therefore a number of animal models reproducing the human disease have been developed

Journal of neural transmission. Rubio, T. Leonhardt, N. Reymann and H. Bittiger GABA receptor antagonists: potential new anti-absence drugs, C. Marescaux, M. Vergnes and R. Bernasconi GABA receptors in rats with spontaneous generalized nonconvulsive epilepsy, A. R. Knight and N. G. Bowery. Personal Name: Marescaux, . 1951-. Personal Name: Vergnes, . 1935-. Personal Name: Bernasconi, . 1929-. Uncontrolled Related/Analytical Title: Generalized nonconvulsive epilepsy. Uniform Title: Journal of neural transmission. Supplementum ; 35. Rubrics

Marescaux, M. Vergnes, and R. Bernasconi (ed. Generalized Non-Convulsive Epilepsy: Focus on GABA-B Receptors Springer-Verlag Wien New York. Dr. C. Marescaux Clinique Neurologique, Hopital Civil, Strasbourg, France. Brain Res 1498-64-72 Depaulis A, Liu Z, Vergnes M, Marescaux C, Micheletti G, Warter JM (1990) Suppression of spontaneous generalized non-convulsive seizures in the rat by.

Generalized Non Convulsive Epilepsy : Focus on Gaba-B Receptors.

Generalized Non-Convulsive Epilepsy: Focus on GABA-B Receptors. 85,92 €. Neuropsychiatric Symptoms of Cerebrovascular Diseases. 156,23 €. Pharmacology of Mitochondria. Age-associated Neurological Diseases. by. Journal of Neural Transmission. J neural transm-supp. NSC 5027 16-7-01 Cyaan Magenta Geel Zwart pharmacological data, the GAERS strain is a well-characterized genetic model of human idiopathic generalized absence epilepsy (Marescaux et a. 1992). Indeed, like in humans (Inouye et a. 1990; Loiseau, 1992; Mirsky et a. 1986; Niedermeyer, 1982; Passouant, 1991), absence attacks occur during quiet wakefulness or drowsiness and rarely during active arousal or sleep ( Drinkenburg et a. 1991; Jando et a. 1995; Lannes et a. 1988 ).

GABA can influence the development of neural progenitor cells via brain-derived neurotrophic factor (BDNF) expression Beyond the nervous system. mRNA expression of the embryonic variant of the GABA-producing enzyme GAD67 in a coronal brain section of a one-day-old Wistar rat, with the highest expression in subventricular zone (svz). Generalized Non-Convulsive Epilepsy: Focus on GABA-B Receptors, C. Vergnes, R. Bernasconi. Ffrench-Constant RH, Rocheleau TA, Steichen JC, Chalmers AE (June 1993). A point mutation in a Drosophila GABA receptor confers insecticide resistance". Journal of Pediatric Epilepsy.

receptor γ2 subunit in a family with generalized epilepsy with febrile seizures plus, American Journal of Human Genetics, vol. 70, no. 2, pp. 530–536, 2002. View at Publisher · View at Google Scholar · View at Scopus. L. Danober, C. Deransart, A. Depaulis, M. Vergnes, and C. Marescaux, Pathophysiological mechanisms of genetic absence epilepsy in the rat, Progress in Neurobiology, vol. 55, no. 1, pp. 27–57, 1998.

Vergnes M, Marescaux C. (1998) Pathophysiological mechanisms of genetic absence epilepsy in the rat. Prog Neurobiol 55:27–57. 1992) GABA receptors in rats with spontaneous generalized nonconvulsive epilepsy. J Neural Transm Suppl 35:189–196. Marescaux C. (1991) Evidence for a critical role of GABAergic transmission within the thalamus in the genesis and control of absence seizures in the rat. Brain Res 545:1–7. OpenUrl CrossRef PubMed.

Generalized non convulsive epilepsy (GNCE), also called absence or petit mal epilepsy, is a disease appearing during childhood. EEG, clinical, pharmacological 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 be resolved in studies that focus on humans. Therefore a number of animal models reproducing the human disease have been developed. The aim of this supplementum is to characterize such models in rodents. First, recent models are extensively described. These include the genetic model of spontaneous GNCE in Strasbourg's Wistar rats and in tottering mice as well as bilateral spike and wave discharges induced by GHB, PTZ or GABA mimetics. Second, this 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, pharmacological, biochemical, metabolic, ionic and molecular data. This supplementum provides an original multidisciplinary approach to the mechanisms involved in GNCE and demonstrates that rodent models are a promising tool which complements the classical feline penicillin model.