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Cerebral Cortex Advance Access published online on March 10, 2009
Cerebral Cortex, doi:10.1093/cercor/bhn237
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Published by Oxford University Press 2009.

Inactivation of the Somatosensory Cortex Prevents Paroxysmal Oscillations in Cortical and Related Thalamic Neurons in a Genetic Model of Absence Epilepsy

Pierre-Olivier Polack1,2, Séverine Mahon1,2, Mario Chavez3 and Stéphane Charpier1,2,4

1 INSERM UMR_S 667, Dynamique et Physiopathologie des Réseaux Neuronaux, F-75005 Paris, France, 2 Collège de France, UMR_S 667, F-75005 Paris, France, 3 Laboratoire de Neurosciences Cognitives & Imagerie Cérébrale, CNRS UPR 640 – LENA, 75651 Paris Cedex 13, France, 4 UPMC Univ Paris 06, UMR_S 667, F-75005 Paris, France

Address correspondence to Stephane Charpier, PhD, Institut National de la Santé et de la Recherche Médicale – Unité 667, Collège de France, 11, place Marcelin Berthelot, 75231 Paris, Cedex 05, France. Email: stephane.charpier{at}college-de-france.fr.

Absence seizures consist of bilateral spike-and-wave discharges (SWDs) occurring over widespread cortical and thalamic regions. In genetic models of absence epilepsy, recent in vivo investigations indicate that SWDs emerge first in the facial somatosensory cortex and then propagate via the corticothalamocortical loop. The specific involvement of this cortical region in ictogenic processes remained to be established and the participation of its related thalamocortical system in seizure initiation remained unclear. Here, using electrocorticographic (ECoG) and intracellular recordings in vivo from cortex and thalamus in the Genetic Absence Epilepsy Rat from Strasbourg (GAERS), we obtained novel evidence for the cortical focus theory of absence epilepsy. We report that blockade of action potential discharge and synaptic activities in facial somatosensory cortical neurons, by topical application of tetrodotoxin, prevents the occurrence of paroxysmal activities in local and distant cortical neurons and ECoGs, as well as in thalamocortical neurons in register with the somatosensory cortex. In contrast, pharmacological inhibition of a remote motor cortical region or of the related thalamic nuclei did not suppress ictal activities in the somatosensory cortex. This study demonstrates that SWDs in GAERS have a focal origin within the facial somatosensory cortex, which is sufficient and necessary to generate ictal activities.

Key Words: absence epilepsy • cortical inactivation • in vivo • somatosensory cortex • thalamus


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