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Neural Plasticity
Volume 7, Issue 1-2, Pages 9-18

The GABA-Withdrawal Syndrome: A Model of Local Status Epilepticus

1Laboratoire de Génétique de la Neurotransmission et des Processus Neurodégénératifs, UMR 9923, CNRS., Paris 75634 , France
2Institut Alfred Fessard, CNRS., Gif sur Yvette 91198, France
3Laboratoire d'Epilepsie Expérimentale, UMR 9923, CNRS., Faculté Pitié-Salpétrière, 91 bd. de l'Hôpital, Paris Cedex 13 75634, France

Copyright © 2000 Hindawi Publishing Corporation. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


The GABA-withdrawal syndrome (GWS) is a model of local status epilepticus following the interruption of a chronic GABA infusion into the rat somatomotor cortex. GWS is characterized by focal epileptic electroencephalographic discharges and associated contralateral myoclonus. In neocorticai slices obtained from GWS rats, most neurons recorded in the GABA-infused area are pyramidal neurons presenting bursting properties. The bursts are induced by white-matter stimulation and/or intracellular depolarizing current injection and correlate with a decrease of cellular sensitivity to GABA, caused by its prolonged infusion. This effect is related to a calcium influx that may reduce the GABAA receptormediated inward current and is responsible for the bursting properties. Here we present evidence for the involvement of calcium- and NMDA-induced currents in burst genesis. We also report modulatory effects of noradrenaline appearing as changes on firing patterns of bursting and nonbursting cells. Complementary histochemical data reveal the existence of a local noradrenergic hyperinnervation and an ectopic expression of tyrosine hydroxylase mRNAs in the epileptic zone.