Generalized Non-Convulsive Epilepsy: Focus on GABA-B Receptors

1. Front Matter

   Pages I-VII

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2. Human absence epilepsies

   • P. Loiseau

   Pages 1-6

3. Pharmacological models of generalized absence seizures in rodents

   • O. Carter Snead III

   Pages 7-19

4. The tottering mouse: a critical review of its usefulness in the study of the neuronal mechanisms underlying epilepsy

   • G. K. Kostopoulos

   Pages 21-36

5. Genetic absence epilepsy in rats from Strasbourg — A review

   • C. Marescaux, M. Vergnes, A. Depaulis

   Pages 37-69

6. Cortical and thalamic lesions in rats with genetic absence epilepsy

   • M. Vergnes, C. Marescaux

   Pages 71-83

7. Role of the thalamic reticular nucleus in the generation of rhythmic thalamo-cortical activities subserving spike and waves

   • G. Avanzini, M. de Curtis, C. Marescaux, F. Panzica, R. Spreafico, M. Vergnes

   Pages 85-95

8. Responses to N-methyl-D-aspartate are enhanced in rats with Petit Mal-like seizures

   • R. Pumain, J. Louvel, M. Gastard, I. Kurcewicz, M. Vergnes

   Pages 97-108

9. Possible mechanisms underlying hyperexcitability in the epileptic mutant mouse tottering

   • G. K. Kostopoulos, C. T. Psarropoulou

   Pages 109-124

10. The inhibitory control of the substantia nigra over generalized non-convulsive seizures in the rat

    • A. Depaulis

    Pages 125-139

11. Mapping of cerebral energy metabolism in rats with genetic generalized nonconvulsive epilepsy

    • A. Nehlig, M. Vergnes, C. Marescaux, S. Boyet

    Pages 141-153

12. Experimental absence seizures: potential role of γ-hydroxybutyric acid and GABAB receptors

    • R. Bernasconi, J. Lauber, C. Marescaux, M. Vergnes, P. Martin, V. Rubio et al.

    Pages 155-177

13. GABAB receptor antagonists: potential new anti-absence drugs

    • C. Marescaux, M. Vergnes, R. Bernasconi

    Pages 179-188

14. GABA receptors in rats with spontaneous generalized nonconvulsive epilepsy

    • A. R. Knight, N. G. Bowery

    Pages 189-196

15. Back Matter

    Pages 197-200

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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.

• Epilepsie
• GABA
• electroencephalography (EEG)
• metabolism
• pathophysiology
• physiology
• research

• Clinique Neurologique, Hôpital Civil, Strasbourg, France

  C. Marescaux

• Centre de Neurochimie, C.N.R.S., Strasbourg, France

  M. Vergnes

• Pharma Division, Ciba-Geigy AG, Basel, Switzerland

  R. Bernasconi

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