scholarly journals Correction: Acute inhibition of neurosteroid estrogen synthesis suppresses status epilepticus in an animal model

eLife ◽  
2016 ◽  
Vol 5 ◽  
Author(s):  
Satoru M Sato ◽  
Catherine S Woolley
2018 ◽  
Vol 29 (7) ◽  
pp. 757-770 ◽  
Author(s):  
Nikita Nirwan ◽  
Preeti Vyas ◽  
Divya Vohora

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.


Epilepsia ◽  
2008 ◽  
Vol 42 (2) ◽  
pp. 171-180 ◽  
Author(s):  
Pavel Kršek ◽  
Anna Mikulecká ◽  
Rastislav Druga ◽  
Zdeněk Hliňák ◽  
Hana Kubová ◽  
...  

Epilepsia ◽  
2003 ◽  
Vol 42 ◽  
pp. 171-180
Author(s):  
Pavel Kršek ◽  
Anna Mikulecká ◽  
Rastislav Druga ◽  
Zdeněk Hliňák ◽  
Hana Kubová ◽  
...  

Heliyon ◽  
2020 ◽  
Vol 6 (7) ◽  
pp. e04557
Author(s):  
Iman Imtiyaz Ahmed Juvale ◽  
Ahmad Tarmizi Che Has

eLife ◽  
2016 ◽  
Vol 5 ◽  
Author(s):  
Satoru M Sato ◽  
Catherine S Woolley

Status epilepticus (SE) is a common neurological emergency for which new treatments are needed. In vitro studies suggest a novel approach to controlling seizures in SE: acute inhibition of estrogen synthesis in the brain. Here, we show in rats that systemic administration of an aromatase (estrogen synthase) inhibitor after seizure onset strongly suppresses both electrographic and behavioral seizures induced by kainic acid (KA). We found that KA-induced SE stimulates synthesis of estradiol (E2) in the hippocampus, a brain region commonly involved in seizures and where E2 is known to acutely promote neural activity. Hippocampal E2 levels were higher in rats experiencing more severe seizures. Consistent with a seizure-promoting effect of hippocampal estrogen synthesis, intra-hippocampal aromatase inhibition also suppressed seizures. These results reveal neurosteroid estrogen synthesis as a previously unknown factor in the escalation of seizures and suggest that acute administration of aromatase inhibitors may be an effective treatment for SE.


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