Abstract
The genetic rat models such as rats of the WAG/Rij strain and GAERS were developed as models for generalized genetic epilepsy and in particular for childhood absence epilepsy. These animal models were described in the eighties of the previous century and both models have, among others, face, construct and predictive validity. Both models were and are currently used as models to predict the action of antiepileptic medication and other experimental treatments, to elucidate neurobiological mechanisms of spike-wave discharges and epileptogenesis. Although the electroencephalagram (EEG)/electrocorticogram (ECoG) is imperative for establishing absence seizures and to quantify the for absence epilepsy typical spike-wave discharges, monitoring the animals behavior is equally necessary. Here an overview is given regarding the design of drug evaluation studies, which animals to use, classical and new EEG variables, the monitoring and quantification of the behavior of the rats, some pitfalls regarding the interpretation of the data, and some developments in EEG technology.
Highlights
Predictive validity is the key word in preclinical animal models
The outcomes of the studies in the models can be considered as correct predictions, since these antiepileptic drugs suppress dose and time dependently, absence seizures, better, the more quantifiable EEG hallmarks of absences, spike-wave discharges (SWDs) in the models
Since very few new antiepileptic drugs were introduced in the market, and none new antiepileptic drugs were specific aimed for the treatment of absence epilepsy
Summary
Predictive validity is the key word in preclinical animal models This implies that results of putative new treatment in humans, often new drugs, can be predicted correctly based on results obtained in the models. This was illustrated in the GAERS and WAG/Rij models by showing that the classical anti-absence drugs such as ETX and VPA, as well as benzodiazepines, correctly predicted their action in patients with absences. Drug Effects on Electrocorticographic Activity sodium channel blockers, such as lamotrigine and the classical anticonvulsants phenytoin and carbamazepine These results as obtained in the genetic models can be considered as correct rejections based on predictions from the models. The models are used to predict the effects of new T-type channel blockers (Tringham et al, 2012; Remen et al, 2016), for the study of antiepileptogenesis (Blumenfeld et al, 2008; Sarkisova et al, 2010; van Luijtelaar et al, 2013; Russo et al, 2016; Leo et al., 2019), for the odyssey toward ultimate causes of absence epilepsy in this model, and for experimental treatment techniques for absence epilepsy such as various types of non-invasive and invasive electrical or magnetic stimulation (Godlevsky et al, 2006; van Luijtelaar and Zobeiri, 2014; van Luijtelaar et al, 2017)
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