Status Epilepticus - Lessons and Challenges from Animal Models

2017 ◽  
pp. 3-17
Author(s):  
Inna Keselman ◽  
Claude G. Wasterlain ◽  
Jerome Niquet ◽  
James W. Y. Chen
Keyword(s):  
Status Epilepticus ◽  
Animal Models

Amygdaloid complex anatomopathological findings in animal models of status epilepticus

2019 ◽  
pp. 106831 ◽  
Author(s):  
Cristiane Queixa Tilelli ◽  
Larissa Ribeiro Flôres ◽  
Vinicius Rosa Cota ◽  
Olagide Wagner de Castro ◽  
Norberto Garcia-Cairasco
Keyword(s):  
Status Epilepticus ◽  
Animal Models ◽  
Amygdaloid Complex

Age-Dependent Consequences of Status Epilepticus: Animal Models

Epilepsia ◽  
2007 ◽  
Vol 48 (s2) ◽  
pp. 75-82 ◽  
Author(s):  
Morris H. Scantlebury ◽  
James G. Heida ◽  
Henry J. Hasson ◽  
Jana Velíšková ◽  
Libor Velíšek ◽  
...  
Keyword(s):  
Status Epilepticus ◽  
Animal Models ◽  
Age Dependent

Animal models of status epilepticus and temporal lobe epilepsy: a narrative review

2018 ◽  
Vol 29 (7) ◽  
pp. 757-770 ◽  
Author(s):  
Nikita Nirwan ◽  
Preeti Vyas ◽  
Divya Vohora
Keyword(s):  
Animal Model ◽  
Status Epilepticus ◽  
Animal Models ◽  
Temporal Lobe Epilepsy ◽  
Temporal Lobe ◽  
Current Literature ◽  
Clinical Characteristics ◽  
Genetic Models ◽  
Suitable Animal Model ◽  
Effective Models

Abstract Temporal lobe epilepsy (TLE) is the chronic and pharmacoresistant form of epilepsy observed in humans. The current literature is insufficient in explicating the comprehensive mechanisms underlying its pathogenesis and advancement. Consequently, the development of a suitable animal model mimicking the clinical characteristics is required. Further, the relevance of status epilepticus (SE) to animal models is dubious. SE occurs rarely in people; most epilepsy patients never experience it. The present review summarizes the established animal models of SE and TLE, along with a brief discussion of the animal models that have the distinctiveness and carries the possibility to be developed as effective models for TLE. The review not only covers the basic requirements, mechanisms, and methods of induction of each model but also focuses upon their major limitations and possible modifications for their future use. A detailed discussion on chemical, electrical, and hypoxic/ischemic models as well as a brief explanation on the genetic models, most of which are characterized by development of SE followed by neurodegeneration, is presented.

scholarly journals Galanin Modulation of Seizures and Seizure Modulation of Hippocampal Galanin in Animal Models of Status Epilepticus

1998 ◽  
Vol 18 (23) ◽  
pp. 10070-10077 ◽  
Author(s):  
Andrey M. Mazarati ◽  
Hantao Liu ◽  
Ursel Soomets ◽  
Raman Sankar ◽  
Don Shin ◽  
...  
Keyword(s):  
Status Epilepticus ◽  
Animal Models

scholarly journals mTOR inhibitor improves autistic-like behaviors related to Tsc2 haploinsufficiency but not following developmental status epilepticus

2021 ◽  
Vol 13 (1) ◽  
Author(s):  
Tomas Petrasek ◽  
Iveta Vojtechova ◽  
Ondrej Klovrza ◽  
Klara Tuckova ◽  
Cestmir Vejmola ◽  
...  
Keyword(s):  
Status Epilepticus ◽  
Social Behavior ◽  
Animal Models ◽  
Mtor Inhibitor ◽  
Genetic Disorder ◽  
Mtor Inhibitors ◽  
Autism Spectrum ◽  
Developmental Status ◽  
Phase Ii Studies ◽  
Eeg Abnormalities

Abstract Background Tuberous sclerosis complex (TSC), a multi-system genetic disorder often associated with autism spectrum disorder (ASD), is caused by mutations of TSC1 or TSC2, which lead to constitutive overactivation of mammalian target of rapamycin (mTOR). In several Tsc1+/- and Tsc2+/- animal models, cognitive and social behavior deficits were reversed by mTOR inhibitors. However, phase II studies have not shown amelioration of ASD and cognitive deficits in individuals with TSC during mTOR inhibitor therapy. We asked here if developmental epilepsy, common in the majority of individuals with TSC but absent in most animal models, could explain the discrepancy. Methods At postnatal day P12, developmental status epilepticus (DSE) was induced in male Tsc2+/- (Eker) and wild-type rats, establishing four experimental groups including controls. In adult animals (n = 36), the behavior was assessed in the paradigms of social interaction test, elevated plus-maze, light-dark test, Y-maze, and novel object recognition. The testing was carried out before medication (T1), during a 2-week treatment with the mTOR inhibitor everolimus (T2) and after an 8-week washing-out (T3). Electroencephalographic (EEG) activity was recorded in a separate set of animals (n = 18). Results Both Tsc2+/- mutation and DSE caused social behavior deficits and epileptiform EEG abnormalities (T1). Everolimus led to a persistent improvement of the social deficit induced by Tsc2+/-, while deficits related to DSE did not respond to everolimus (T2, T3). Conclusions These findings may contribute to an explanation why ASD symptoms in individuals with TSC, where comorbid early-onset epilepsy is common, were not reliably ameliorated by mTOR inhibitors in clinical studies.

scholarly journals Treatment of early life status epilepticus: What can we learn from animal models?

2018 ◽  
Vol 3 (S2) ◽  
pp. 169-179 ◽  
Author(s):  
Kerry W. Thompson ◽  
Lucie Suchomelova ◽  
Claude G. Wasterlain
Keyword(s):  
Status Epilepticus ◽  
Animal Models ◽  
Early Life
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