Commonalities and differences in extracellular levels of hippocampal acetylcholine and amino acid neurotransmitters during status epilepticus and subsequent epileptogenesis in two rat models of temporal lobe epilepsy

2019 ◽  
Vol 1712 ◽  
pp. 109-123 ◽  
Author(s):  
Sebastian Meller ◽  
Claudia Brandt ◽  
Wiebke Theilmann ◽  
Jochen Klein ◽  
Wolfgang Löscher
Keyword(s):  
Status Epilepticus ◽  
Amino Acid ◽  
Temporal Lobe Epilepsy ◽  
Temporal Lobe ◽  
Amino Acid Neurotransmitters ◽  
Rat Models

Prophylactic treatment with melatonin after status epilepticus: Effects on epileptogenesis, neuronal damage, and behavioral changes in a kainate model of temporal lobe epilepsy

2013 ◽  
Vol 27 (1) ◽  
pp. 174-187 ◽  
Author(s):  
Jana Tchekalarova ◽  
Zlatina Petkova ◽  
Daniela Pechlivanova ◽  
Slavianka Moyanova ◽  
Lidia Kortenska ◽  
...  
Keyword(s):  
Status Epilepticus ◽  
Temporal Lobe Epilepsy ◽  
Temporal Lobe ◽  
Prophylactic Treatment ◽  
Neuronal Damage ◽  
Behavioral Changes

scholarly journals Induction of the Nrf2 Pathway by Sulforaphane Is Neuroprotective in a Rat Temporal Lobe Epilepsy Model

Antioxidants ◽  
2021 ◽  
Vol 10 (11) ◽  
pp. 1702
Author(s):  
Sereen Sandouka ◽  
Tawfeeq Shekh-Ahmad
Keyword(s):  
Oxidative Stress ◽  
Cell Death ◽  
Status Epilepticus ◽  
Temporal Lobe Epilepsy ◽  
Antioxidant Capacity ◽  
Temporal Lobe ◽  
Epileptiform Activity ◽  
Neuronal Cell Death ◽  
Neuronal Cell ◽  
The Brain

Epilepsy is a chronic disease of the brain that affects over 65 million people worldwide. Acquired epilepsy is initiated by neurological insults, such as status epilepticus, which can result in the generation of ROS and induction of oxidative stress. Suppressing oxidative stress by upregulation of the transcription factor, nuclear factor erythroid 2-related factor 2 (Nrf2) has been shown to be an effective strategy to increase endogenous antioxidant defences, including in brain diseases, and can ameliorate neuronal damage and seizure occurrence in epilepsy. Here, we aim to test the neuroprotective potential of a naturally occurring Nrf2 activator sulforaphane, in in vitro epileptiform activity model and a temporal lobe epilepsy rat model. Sulforaphane significantly decreased ROS generation during epileptiform activity, restored glutathione levels, and prevented seizure-like activity-induced neuronal cell death. When given to rats after 2 h of kainic acid-induced status epilepticus, sulforaphane significantly increased the expression of Nrf2 and related antioxidant genes, improved oxidative stress markers, and increased the total antioxidant capacity in both the plasma and hippocampus. In addition, sulforaphane significantly decreased status epilepticus-induced neuronal cell death. Our results demonstrate that Nrf2 activation following an insult to the brain exerts a neuroprotective effect by reducing neuronal death, increasing the antioxidant capacity, and thus may also modify epilepsy development.

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.

Status Epilepticus-Induced Neurogenesis and Neuron Loss in the Kainate Model of Temporal Lobe Epilepsy

2003 ◽  
Vol 21 (2) ◽  
pp. 157-166
Author(s):  
Takashi Ninomiya ◽  
Kiyoshi Morimoto ◽  
Takemi Watanabe ◽  
Tohru Hirao ◽  
Osamu Yasuhara ◽  
...  
Keyword(s):  
Status Epilepticus ◽  
Temporal Lobe Epilepsy ◽  
Temporal Lobe ◽  
Neuron Loss
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