scholarly journals Cortical epileptogenesis of slowly kindled freely moving rats

2014 ◽  
Vol 60 (6) ◽  
pp. 249-253
Author(s):  
K. Orbán-Kis ◽  
Iringó Száva ◽  
T. Szilágyi
Keyword(s):  
Temporal Lobe Epilepsy ◽  
Temporal Lobe ◽  
Hippocampal Formation ◽  
Field Potential ◽  
Bipolar Electrode ◽  
Freely Moving Rats ◽  
Spontaneous Seizures ◽  
Freely Moving ◽  
Negative Field

Abstract Objective. Epilepsy is a neurological disorder that can be caused by many underlying pathologies. The epileptic and interictal manifestations that appear during the progression of chronic epilepsy are still not understood completely. One of the most frequent forms of this disease is temporal lobe epilepsy in which is clear involvement of the hippocampal formation. In order to study the electrografic progression of untreated seizures we used amygdala kindling in freely moving rats. Methods. Seven animals were implanted with bilateral hippocampal and prefrontal electrodes. A bipolar electrode, implanted in the lateral nuclei of the left amygdala was used for stimulation. The kindled group of animals was stimulated daily with the minimum current intensity needed to reach the afterdischarge threshold. Behavioral changes during kindling were scored according to the Racine scale. Results. The average seizure severity on the Racine scale was 2.6±0.4 by day 6 and 4.4±0.6 by day 20. The first spontaneous seizures appeared after 31 days of stimulation. During spontaneous seizures the preictal spike full width at half maximum increased gradually from 51±4msec to 110±5msec (p < 0.05) whereas the amplitude of the negative field potential deflection increased by 62% (p < 0.05). Conclusions. Our study showed that the progression of temporal lobe epilepsy, as seen in humans, can be reproduced in the kindling model with high fidelity. This study confirms in vivo the increase in preictal spike duration as well as the increase of the amplitude of negative field potential deflection during the preictal period.

Stimulation of the Parasubiculum Modulates Entorhinal Cortex Responses to Piriform Cortex Inputs In Vivo

2004 ◽  
Vol 92 (2) ◽  
pp. 1226-1235 ◽  
Author(s):  
Douglas A. Caruana ◽  
C. Andrew Chapman
Keyword(s):  
Entorhinal Cortex ◽  
Hippocampal Formation ◽  
Piriform Cortex ◽  
Current Source ◽  
Field Potential ◽  
Implanted Electrodes ◽  
Deep Layers ◽  
Negative Field ◽  
Stimulation Of

Although a major output of the hippocampal formation is from the subiculum to the deep layers of the entorhinal cortex, the parasubiculum projects to the superficial layers of the entorhinal cortex and may therefore modulate how the entorhinal cortex responds to sensory inputs from other cortical regions. Recordings at multiple depths in the entorhinal cortex were first used to characterize field potentials evoked by stimulation of the parasubiculum in urethan-anesthetized rats. Current source density analysis showed that a prominent surface-negative field potential component is generated by synaptic activation in layer II. The surface-negative field potential was also observed in rats with chronically implanted electrodes. The response was maintained during short stimulation trains of ≤125 Hz, suggesting that it is generated by activation of monosynaptic inputs to the entorhinal cortex. The piriform cortex also projects to layer II of the entorhinal cortex, and interactions between parasubicular and piriform cortex inputs were investigated using double-site stimulation tests. Simultaneous activation of parasubicular and piriform cortex inputs with high-intensity pulses resulted in smaller synaptic potentials than were expected on the basis of summing the individual responses, consistent with the termination of both pathways onto a common population of neurons. Paired-pulse tests were then used to assess the effect of parasubicular stimulation on responses to piriform cortex stimulation. Responses of the entorhinal cortex to piriform cortex inputs were inhibited when the parasubiculum was stimulated 5 ms earlier and were enhanced when the parasubiculum was stimulated 20–150 ms earlier. These results indicate that excitatory inputs to the entorhinal cortex from the parasubiculum may enhance the propagation of neuronal activation patterns into the hippocampal circuit by increasing the responsiveness of the entorhinal cortex to appropriately timed inputs.

scholarly journals A systems approach delivers a functional microRNA catalog and expanded targets for seizure suppression in temporal lobe epilepsy

2020 ◽  
Vol 117 (27) ◽  
pp. 15977-15988 ◽  
Author(s):  
Morten T. Venø ◽  
Cristina R. Reschke ◽  
Gareth Morris ◽  
Niamh M. C. Connolly ◽  
Junyi Su ◽  
...  
Keyword(s):  
Temporal Lobe Epilepsy ◽  
Temporal Lobe ◽  
Antisense Oligonucleotides ◽  
Systems Approach ◽  
Brain Structures ◽  
Proteomic Data ◽  
Common Drug ◽  
Spontaneous Seizures ◽  
Resistant Form

Temporal lobe epilepsy is the most common drug-resistant form of epilepsy in adults. The reorganization of neural networks and the gene expression landscape underlying pathophysiologic network behavior in brain structures such as the hippocampus has been suggested to be controlled, in part, by microRNAs. To systematically assess their significance, we sequenced Argonaute-loaded microRNAs to define functionally engaged microRNAs in the hippocampus of three different animal models in two species and at six time points between the initial precipitating insult through to the establishment of chronic epilepsy. We then selected commonly up-regulated microRNAs for a functional in vivo therapeutic screen using oligonucleotide inhibitors. Argonaute sequencing generated 1.44 billion small RNA reads of which up to 82% were microRNAs, with over 400 unique microRNAs detected per model. Approximately half of the detected microRNAs were dysregulated in each epilepsy model. We prioritized commonly up-regulated microRNAs that were fully conserved in humans and designed custom antisense oligonucleotides for these candidate targets. Antiseizure phenotypes were observed upon knockdown of miR-10a-5p, miR-21a-5p, and miR-142a-5p and electrophysiological analyses indicated broad safety of this approach. Combined inhibition of these three microRNAs reduced spontaneous seizures in epileptic mice. Proteomic data, RNA sequencing, and pathway analysis on predicted and validated targets of these microRNAs implicated derepressed TGF-β signaling as a shared seizure-modifying mechanism. Correspondingly, inhibition of TGF-β signaling occluded the antiseizure effects of the antagomirs. Together, these results identify shared, dysregulated, and functionally active microRNAs during the pathogenesis of epilepsy which represent therapeutic antiseizure targets.

scholarly journals Relevance of Removal of Limbic Structures in Surgery for Temporal Lobe Epilepsy

1991 ◽  
Vol 18 (S4) ◽  
pp. 628-635 ◽  
Author(s):  
André Olivier
Keyword(s):  
Temporal Lobe Epilepsy ◽  
Temporal Lobe ◽  
Clinical Evidence ◽  
Hippocampal Formation ◽  
Clinical Work ◽  
Limbic Structures

ABSTRACT:We have briefly reviewed the experimental and clinical evidence for the importance of the amygdala and hippocampal formation in temporal lobe epilepsy. More specifically, we have analyzed our own experience in patients with temporal lobe epilepsy investigated with intracerebral stereotaxic electrodes and operated by various modalities of resection. Our results, in agreement with previous experimental and clinical work, provide further evidence for an overwhelming predominance of limbic participation in temporal lobe epilepsy. As a result, more and more selective procedures are being carried out involving the mesial structures. However, this shift has been slow and progressive because of the proven value of cortico-amygdalo-hippocampectomy which provides excellent results on seizure tendency with low morbidity.

Elevated caudate DOPA decarboxylase activity in vivo in schizophrenia and temporal lobe epilepsy with psychosis

1991 ◽  
Vol 1 (3) ◽  
pp. 472 ◽  
Author(s):  
J Reith ◽  
C Benkelfat ◽  
H Kuwabara ◽  
G Savard ◽  
G Chouinard ◽  
...  
Keyword(s):  
Temporal Lobe Epilepsy ◽  
Temporal Lobe ◽  
Dopa Decarboxylase ◽  
Decarboxylase Activity
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