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The Journal of Neuroscience, June 13, 2007, 27(24):6590-6599; doi:10.1523/JNEUROSCI.0753-07.2007

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Neurobiology of Disease
Deep Layer Somatosensory Cortical Neurons Initiate Spike-and-Wave Discharges in a Genetic Model of Absence Seizures

Pierre-Olivier Polack,¹ Isabelle Guillemain,² Emilie Hu,^1,3 Colin Deransart,² Antoine Depaulis,² and Stéphane Charpier^1,3

¹Institut National de la Santé et de la Recherche Médicale Unité 667, Collège de France, 75231 Paris, Cedex 05, France, ²Institut National de la Santé et de la Recherche Médicale Unité 836–Université Joseph Fourier–Commissariat à l'Energie Atomique–Centre Hospitalier Universitaire, Institut des Neurosciences BP53, 38041 Grenoble Cedex 9, France, and ³Université Pierre et Marie Curie, 75005 Paris, France

Correspondence should be addressed to Pierre-Olivier Polack, 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: pierre-olivier.polack{at}college-de-france.fr

Typical absence has long been considered as the prototypic form of generalized nonconvulsive epileptic seizures. Recent investigations in patients and animal models suggest that absence seizures could originate from restricted regions of the cerebral cortex. However, the cellular and local network processes of seizure initiation remain unknown. Here, we show that absence seizures in Genetic Absence Epilepsy Rats from Strasbourg, a well established genetic model of this disease, arise from the facial somatosensory cortex. Using in vivo intracellular recordings, we found that epileptic discharges are initiated in layer 5/6 neurons of this cortical region. These neurons, which show a distinctive hyperactivity associated with a membrane depolarization, lead the firing of distant cortical cells during the epileptic discharge. Consistent with their ictogenic properties, neurons from this "focus" exhibit interictal and preictal oscillations that are converted into epileptic pattern. These results confirm and extend the "focal hypothesis" of absence epilepsy and provide a cellular scenario for the initiation and generalization of absence seizures.

Key words: absence epilepsy; somatosensory cortex; thalamus; cortical synchronization; in vivo; focal epilepsy

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Received Feb. 19, 2007; revised May 7, 2007; accepted May 8, 2007.

Correspondence should be addressed to Pierre-Olivier Polack, 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: pierre-olivier.polack{at}college-de-france.fr

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Are absence-related epileptic discharges initiated by layer V or layer VI neurons?

Didier Pinault

J. Neurosci. Online, 15 Jul 2007 [Full text]

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