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Cereb Cortex. 2017 Sep 1;27(9):4607-4623. doi: 10.1093/cercor/bhx174.

Building Up Absence Seizures in the Somatosensory Cortex: From Network to Cellular Epileptogenic Processes.

Author information

1
Univ. Grenoble Alpes, Grenoble Institut des Neurosciences, GIN, F-38000 Grenoble, France.
2
Inserm, U1216, F-38000 Grenoble, France.
3
Inserm U 1127, CNRS UMR 7225, Sorbonne Universités, UPMC Univ Paris 06 UMR S 1127, Institut du Cerveau et de la Moelle épinière, ICM, F-75013, Paris, France.
4
Pediatric Neurosurgery Department, Fondation Ophtalmologique A. de Rothschild, 75019 Paris, France.
5
CHU de Grenoble, F-38000 Grenoble, France.
6
UPMC Univ Paris 06, F-75005, Paris, France.

Abstract

The epileptogenic processes leading to recurrent seizures in Genetic Epilepsies are largely unknown. Using the Genetic Absence Epilepsy Rat from Strasbourg, we investigated in vivo the network and single neuron mechanisms responsible for the early emergence of epileptic activity. Local field potential recordings in the primary somatosensory cortex (SoCx), from the second post-natal week to adulthood, showed that immature cortical discharges progressively evolved into typical spike-and-wave discharges following a 3-step maturation process. Intracellular recordings from deep-layer SoCx neurons revealed that this maturation was associated with an age-dependent increase in cortical neurons intrinsic excitability, combining a membrane depolarization and an enhancement of spontaneous firing rate with a leftward shift in their input-output relation. These cellular changes were accompanied by a progressive increase in the strength of the local synaptic activity associated with a growing propensity of neurons to generate synchronized oscillations. Chronic anti-absence treatment before the occurrence of mature cortical discharges did not alter epileptogenesis or the drug efficiency at adulthood. These findings demonstrate that recurrent absence seizures originate from the progressive acquisition of pro-ictogenic properties in SoCx neurons and networks during the post-natal period and that these processes cannot be interrupted by early anti-absence treatment.

KEYWORDS:

GAERS; absence epilepsy; early anti-epileptic treatment; epileptogenesis; in vivo intracellular recordings; somatosensory cortex

PMID:
28922856
DOI:
10.1093/cercor/bhx174
[Indexed for MEDLINE]

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