Abstract:
:Absence epilepsy is a form of generalized epilepsy commonly seen in children. The neuronal process by which ethosuximide (ETX), a first choice anti-absence drug, prevents absence seizures is still unresolved. Recent clinical findings have indicated that focal cortical regions are involved during absence seizures. Consistently, it has been shown in genetic models of absence epilepsy that epileptic discharges arise from a delimited region of the cerebral cortex. Here, we made simultaneous in vivo electrocorticographic and intracellular recordings from the cortical focus of the genetic absence epilepsy rat from Strasbourg and examined the effects of systemic injection of ETX at a therapeutic concentration. We show that the interruption of seizures by ETX is correlated with a recovery, in the hyperactive focus neurons, of physiologic values of membrane potential, firing rate, and pattern, as measured in analogous neurons from nonepileptic rats. These data suggest that the anti-absence action of ETX results from the conversion of ictogenic cortical neurons into normal cortical neurons.
journal_name
Epilepsiajournal_title
Epilepsiaauthors
Polack PO,Charpier Sdoi
10.1111/j.1528-1167.2009.02047.xsubject
Has Abstractpub_date
2009-07-01 00:00:00pages
1816-20issue
7eissn
0013-9580issn
1528-1167pii
EPI2047journal_volume
50pub_type
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