Upholding WAG/Rij rats as a model of absence epileptogenesis: Hidden mechanisms and a new theory on seizure development
Publication year
2016Author(s)
Number of pages
21 p.
Source
Neuroscience and Biobehavioral Reviews, 71, (2016), pp. 388-408ISSN
Publication type
Article / Letter to editor
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Organization
SW OZ DCC SMN
Journal title
Neuroscience and Biobehavioral Reviews
Volume
vol. 71
Languages used
English (eng)
Page start
p. 388
Page end
p. 408
Subject
Biological psychology; DI-BCB_DCC_Theme 3: Plasticity and Memory; Biologische psychologieAbstract
The 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 non-genetically 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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- Academic publications [246764]
- Faculty of Social Sciences [30508]
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