Elevated Expression of the Delta-Subunit of Epithelial Sodium Channel in Temporal Lobe Epilepsy Patients and Rat Model

2015 ◽  
Vol 57 (4) ◽  
pp. 510-518 ◽  
Author(s):  
Zhonggui Li ◽  
Xiujuan Mi ◽  
Yan Xiong ◽  
Xin Xu ◽  
Xuefeng Wang ◽  
...  
Keyword(s):  
Temporal Lobe Epilepsy ◽  
Sodium Channel ◽  
Temporal Lobe ◽  
Rat Model ◽  
Epithelial Sodium Channel ◽  
Elevated Expression ◽  
Delta Subunit

Up-regulated ephrinB3/EphB3 expression in intractable temporal lobe epilepsy patients and pilocarpine induced experimental epilepsy rat model

2016 ◽  
Vol 1639 ◽  
pp. 1-12 ◽  
Author(s):  
Hao Huang ◽  
Ruohan Li ◽  
Jinxian Yuan ◽  
Xin Zhou ◽  
Xi Liu ◽  
...  
Keyword(s):  
Temporal Lobe Epilepsy ◽  
Temporal Lobe ◽  
Rat Model ◽  
Experimental Epilepsy

Neuroregenerative Gene Therapy to Treat Temporal Lobe Epilepsy in a Rat Model

2021 ◽  
pp. 102198
Author(s):  
Jiajun Zheng ◽  
Tingjie Li ◽  
Shuang Qi ◽  
Bing Qin ◽  
Jiandong Yu ◽  
...  
Keyword(s):  
Gene Therapy ◽  
Temporal Lobe Epilepsy ◽  
Temporal Lobe ◽  
Rat Model

Imaging of P-glycoprotein-mediated pharmacoresistance in the hippocampus: Proof-of-concept in a chronic rat model of temporal lobe epilepsy

Epilepsia ◽  
2010 ◽  
Vol 51 (9) ◽  
pp. 1780-1790 ◽  
Author(s):  
Hero Bartmann ◽  
Christina Fuest ◽  
Christian La Fougere ◽  
Guoming Xiong ◽  
Theresa Just ◽  
...  
Keyword(s):  
Temporal Lobe Epilepsy ◽  
Temporal Lobe ◽  
Rat Model ◽  
Proof Of Concept ◽  
P Glycoprotein

scholarly journals Effect of chemogenetic modulation of hippocampal neurons on depression and spatial memory impairment in a rat model for temporal lobe epilepsy.

2019 ◽  
Vol 13 ◽  
Author(s):  
Erine Craey ◽  
Marie-Gabrielle Goossens ◽  
Jana Desloovere ◽  
Caroline Merckx ◽  
Chris Van Den Haute ◽  
...  
Keyword(s):  
Temporal Lobe Epilepsy ◽  
Spatial Memory ◽  
Temporal Lobe ◽  
Rat Model ◽  
Hippocampal Neurons ◽  
Memory Impairment

scholarly journals Modulation of miR-146a/complement factor H-mediated inflammatory responses in a rat model of temporal lobe epilepsy

2016 ◽  
Vol 36 (6) ◽  
Author(s):  
Fang He ◽  
Bei Liu ◽  
Qiang Meng ◽  
Yang Sun ◽  
Weiwen Wang ◽  
...  
Keyword(s):  
Temporal Lobe Epilepsy ◽  
Temporal Lobe ◽  
Rat Model ◽  
Inflammatory Responses ◽  
Chronic Phase ◽  
Factor H ◽  
Complement Factor H ◽  
Luciferase Reporter ◽  
Complement Factor ◽  
Small Regulatory Rna

Increasing evidence supports the involvement of inflammatory and immune processes in temporal lobe epilepsy (TLE). miRNAs represent small regulatory RNA molecules that have been shown to act as negative regulators of gene expression controlling different biological processes, including immune system homoeostasis and function. We investigated the expression and cellular distribution of miRNA-146a (miR-146a) in a rat model of TLE. Prominent up-regulation of miR-146a activation was evident in 1 week after status epilepticus (SE) and persisted in the chronic phase. The predicted miR-146a's target complement factor H (CFH) mRNA and protein expression was also down-regulated in TLE rat model. Furthermore, transfection of miR-146a mimics in neuronal and glial cells down-regulated CFH mRNA and protein levels respectively. Luciferase reporter assays demonstrated that miR-146a down-regulated CFH mRNA expression via 3′-UTR pairing. Down-regulating miR-146a by intracerebroventricular injection of antagomir-146a enhanced the hippocampal expression of CFH in TLE model and decreased seizure susceptibility. These findings suggest that immunopathological deficits associated with TLE can in part be explained by a generalized miR-146a-mediated down-regulation of CFH that may contribute to epileptogenesis in a rat model of TLE.

Hippocampal asymmetry: differences in the left and right hippocampus proteome in the rat model of temporal lobe epilepsy

2017 ◽  
Vol 154 ◽  
pp. 22-29 ◽  
Author(s):  
Leila Sadeghi ◽  
Albert Anatolyevich Rizvanov ◽  
Ilnur Ildusovich Salafutdinov ◽  
Bahareh Dabirmanesh ◽  
Mohammad Sayyah ◽  
...  
Keyword(s):  
Temporal Lobe Epilepsy ◽  
Temporal Lobe ◽  
Rat Model ◽  
Left And Right

Responses of Deep Entorhinal Cortex are Epileptiform in an Electrogenic Rat Model of Chronic Temporal Lobe Epilepsy

1998 ◽  
Vol 80 (1) ◽  
pp. 230-240 ◽  
Author(s):  
Nathan B. Fountain ◽  
Jonathan Bear ◽  
Edward H. Bertram ◽  
Eric W. Lothman
Keyword(s):  
Temporal Lobe Epilepsy ◽  
Entorhinal Cortex ◽  
Temporal Lobe ◽  
Rat Model ◽  
Action Potentials ◽  
Nmda Antagonist ◽  
Target Cells ◽  
Excitatory Postsynaptic Potential ◽  
Inhibitory Interneurons ◽  
And Control

Fountain, Nathan B., Jonathan Bear, Edward H. Bertram III, and Eric W. Lothman. Responses of deep entorhinal cortex are epileptiform in an electrogenic rat model of chronic temporal lobe epilepsy. J. Neurophysiol. 80: 230–240, 1998. We investigated whether entorhinal cortex (EC) layer IV neurons are hyperexcitable in the post-selfsustaining limbic status epilepticus (post-SSLSE) animal model of temporal lobe epilepsy. We studied naive rats ( n = 44), epileptic rats that had experienced SSLSE resulting in spontaneous seizures ( n = 45), and electrode controls ( n = 7). There were no differences between electrode control and naive groups, which were pooled into a single control group. Intracellular and extracellular recordings were made from deep layers of EC, targeting layer IV, which was activated by stimulation of the superficial layers of EC or the angular bundle. There were no differences between epileptic and control neurons in basic cellular characteristics, and all neurons were quiescent under resting conditions. In control tissue, 77% of evoked intracellular responses consisted of a short-duration [8.6 ± 1.3 (SE) ms] excitatory postsynaptic potential and a single action potential followed by γ-aminobutyric acid-A (GABAA) and GABAB inhibitory post synaptic potentials (IPSPs). Ten percent of controls did not contain IPSPs. In chronically epileptic tissue, evoked intracellular responses demonstrated prolonged depolarizing potentials (256 ± 39 ms), multiple action potentials (13 ± 4), and no IPSPs. Ten percent of epileptic responses were followed by rhythmic “clonic” depolarizations. Epileptic responses exhibited an all-or-none response to progressive increases in stimulus intensity and required less stimulation to elicit action potentials. In both epileptic and control animals, intracellular responses correlated precisely in morphology and duration with extracellular field potentials. Severing the hippocampus from the EC did not alter the responses. Duration of intracellular epileptic responses was reduced 22% by the N-methyl-d-aspartate (NMDA) antagonist d(−)-2-amino-5-phosphonovaleric acid (APV), but they did not return to normal and IPSPs were not restored. Epileptic and control responses were abolished by the non-NMDA antagonist 6,7-dinitroquinoxaline-2-3-dione (DNQX). A monosynaptic IPSP protocol was used to test connectivity of inhibitory interneurons to primary cells by direct activation of interneurons with a stimulating electrode placed near the recording electrode in the presence of APV and DNQX. Using this protocol, IPSPs similar to control ( P > 0.05) were seen in epileptic cells. The findings demonstrate that deep layer EC cells are hyperexcitable or “epileptiform” in this model. Hyperexcitability is not due to interactions with the hippocampus. It is due partially to augmented NMDA-mediated excitation. The lack of IPSPs in epileptic neurons may suggest inhibition is impaired, but we found evidence that inhibitory interneurons are connected to their target cells and are capable of inducing IPSPs.

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