Unilateral and Bilateral Cortical Resection: Effects on Spike-Wave Discharges in a Genetic Absence Epilepsy Model

Scicchitano, Francesca; Rijn, Clementina M. van; Luijtelaar, Gilles van

doi:10.1371/journal.pone.0133594

Cited by 19 publications

(15 citation statements)

References 79 publications

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“…Therefore, it has been suggested that absence seizures in this strain may in fact, have a bi-lateral focal origin (Luttjohann et al, 2011;Meeren et al, 2002;van Luijtelaar and Sitnikova, 2006). In agreement with this, it has recently been demonstrated that the removal of only both foci completely abolishes SWDs (Scicchitano et al, 2015) while fMRI (functional magnetic resonance imaging) studies have confirmed the presence of bilateral activated regions in the somatosensory cortex . Based on this background, we can then suppose that these focal epileptic areas may be genetically predetermined to be hyperexcitable (D'Antuono et al, 2006;Kole et al, 2007;Luttjohann et al, 2011;Strauss et al, 2004) from a certain developmental age onwards.…”

supporting

confidence: 53%

Upholding WAG/Rij rats as a model of absence epileptogenesis: Hidden mechanisms and a new theory on seizure development

Russo

Citraro

Constanti³

et al. 2016

Neuroscience & Biobehavioral Reviews

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128

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Upholding WAG/Rij rats as a model of absence epileptogenesis: Hidden mechanisms and a new theory on seizure development.Neuroscience and Biobehavioral Reviews http://dx.doi.org/10. 1016/j.neubiorev.2016.09.017 This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain. AbstractThe WAG/Rij rat model has recently gathered attention as a suitable animal model of absence epileptogenesis. This latter term has a broad definition encompassing any possible cause that determines the development of spontaneous seizures; however, most of, if not all, preclinical knowledge on epileptogenesis is confined to the study of post-brain insult models such as traumatic brain injury or post-status epilepticus models. WAG/Rij rats, but also synapsin 2 knockout, Kv7 current-deficient mice represent the first examples of genetic models where an efficacious antiepileptogenic treatment (ethosuximide) was started before seizure onset. In this review, we have critically reconsidered all articles published regarding WAG/Rij rats, from the perspective that the period before SWD onset is considered as the latent period. In our new theory on seizure development, it is proposed that genes might be considered as the initial "insult" responsible for all plastic changes underpinning the development of spontaneous seizures. According to this idea, in WAG/Rij rats, genetic predisposition would lead to the development of abnormal bilateral cortical epileptic foci, which would then nongenetically stimulate the rest of the brain to rearrange networks in order to phenotypically develop seizures similarly to what happens during electrical kindling.

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supporting

confidence: 53%

Upholding WAG/Rij rats as a model of absence epileptogenesis: Hidden mechanisms and a new theory on seizure development

Russo

Citraro

Constanti³

et al. 2016

Neuroscience & Biobehavioral Reviews

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128

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“…Absence seizures in rodents are most prominent in the somatosensory cortices (Meeren et al, 2002;Polack et al, 2007;Scicchitano et al, 2015). We reasoned that if abnormally increased myelination is caused by seizure activity, these changes would be specific to the seizure-affected regions.…”

Section: Myelination Increases Within Corpus Callosum Regions Affectementioning

confidence: 99%

Maladaptive myelination promotes epileptogenesis in absence epilepsy

Knowles

Soane

Frost

et al. 2020

Preprint

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Neuronal activity can influence the generation of new oligodendrocytes (oligodendrogenesis) and myelination. In health, this is an adaptive process that can increase synchrony within distributed neuronal networks and contribute to cognitive function. We hypothesized that in seizure disorders, aberrant neuronal activity may promote maladaptive myelination that contributes to pathogenesis. Absence epilepsy is a disease defined by increasingly frequent behavioral arrest seizures over time, thought to be due to thalamocortical network hypersynchrony. We tested the hypothesis that activity-dependent myelination resulting from absence seizures promotes epileptogenesis. Using two distinct models of absence epilepsy, Wag/Rij rats and Scn8a+/mut mice, we found increased oligodendrogenesis and myelination specifically within the absence seizure network. These changes are evident only after seizure onset in both models and are prevented with pharmacological inhibition of seizures. Genetic blockade of activity-dependent myelination during epileptogenesis markedly decreased seizure frequency in the Scn8a+/mut mouse model of absence epilepsy. Taken together, these findings indicate that activity-dependent myelination driven by absence seizures contributes to seizure kindling during epileptogenesis.

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“…Accordingly, seizures in WAG/Rij rats could have a bilateral focal origin [24][25][26]. Very recently, it has been described as the surgical removal of both foci, in these rats, totally abolished SWDs [24]. According to these evidence, it is possible to hypothesize that these focal epileptic areas could be genetically programmed to become hyperexcitable [25,27,28].…”

Section: The Genetically-programmed Epileptogenic Process In Wag/rij mentioning

confidence: 98%

“…Several studies, performed in WAG/Rij in rats, have affirmed that, in this strain, exists a focally increased excitability in the deep layers of the perioral region of somatosensory cortex, where the SWDs arise. Accordingly, seizures in WAG/Rij rats could have a bilateral focal origin [24][25][26]. Very recently, it has been described as the surgical removal of both foci, in these rats, totally abolished SWDs [24].…”

Section: The Genetically-programmed Epileptogenic Process In Wag/rij mentioning

confidence: 99%

WAG/Rij rat model: a resource for the pharmacology of epileptogenesis and related neurological/psychiatric comorbidities

Leo

Nesci

et al. 2019

Neurosci Res Notes

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The discovery of potential antiseizure drugs (ASDs) requires the use of experimental models that can also provide a unique chance for identifying new effective molecules able to prevent and/or cure epilepsy. Most of the preclinical knowledge on epileptogenesis derives from studies performed on post-insult models that are characterized by a recognizable first insult, a silent period lasting until the onset of the first seizure and a chronic period characterized by spontaneous recurrent seizures (SRSs). At odds, genetic models, in which the first insult remains to be identified, have been poorly investigated. Among the genetic models, the WAG/Rij rat was validated as a suitable experimental model of absence epileptogenesis with neuropsychiatric symptomatology, in which, according to our previous hypothesis on SRSs onset, genes could be considered the first ‘insult’ underlying all plastic modifications supporting the occurrences of absence seizures in this strain. In fact, in several genetic models, the initial insult could be described as the mutation leading to epilepsy that, to date, remains to be defined in this strain. The silent period ends at the occurrence of the first SRS, which is approximately at 2-3 months of age in these rats and after that time the chronic phase initiates, in which, absence seizures increase over time underlying likely further epileptogenic processes. In this review, we describe both the features of this experimental model and the effects of several pharmacological treatments against epileptogenesis and its related comorbidities including depressive-like symptoms and cognitive decline.

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Unilateral and Bilateral Cortical Resection: Effects on Spike-Wave Discharges in a Genetic Absence Epilepsy Model

Cited by 19 publications

References 79 publications

Upholding WAG/Rij rats as a model of absence epileptogenesis: Hidden mechanisms and a new theory on seizure development

Upholding WAG/Rij rats as a model of absence epileptogenesis: Hidden mechanisms and a new theory on seizure development

Maladaptive myelination promotes epileptogenesis in absence epilepsy

WAG/Rij rat model: a resource for the pharmacology of epileptogenesis and related neurological/psychiatric comorbidities

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