Afterdischarge threshold reduction in the kindling model of epilepsy

Ng, Min-Sun Mark; Hwang, Paul A.; Burnham, W. McIntyre

doi:10.1016/j.eplepsyres.2006.06.007

Cited by 11 publications

(6 citation statements)

References 19 publications

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“…Near resemblance of these results with those obtained in the present AK study indicates a similarity of underlying epileptogenic processes initiated by the two kindling paradigms. However in AK, epileptogenesis is triggered in the intact brain with only sensory stimulation that excludes a possible influence of depth electrode implantation described in the electrical kindling model (Loscher et al., 1999; Ng et al., 2006) and emphasizes a role of endogenous factors in the epileptogenic process.…”

Section: Discussionmentioning

confidence: 99%

Audiogenic kindling in Wistar and WAG/Rij rats: Kindling‐prone and kindling‐resistant subpopulations

Vinogradova

2008

Epilepsia

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SUMMARYPurpose: Audiogenic kindling (AK) is a model of naturally occurring epileptogenesis triggered by repeated sound stimulation of rats genetically prone to audiogenic seizures. It is accepted that limbic seizure networks underlie progressive changes in behavioral seizure pattern during AK. The present study investigated AK progression in rats susceptible and unsusceptible to absence seizures. Methods: Progression of AK as indicated by an appearance and intensification of limbic clonus was examined in Wistar Albino Glaxo/Rijswijk (WAG/Rij) rats with genetic absence epilepsy and in Wistar rats. Results: Subpopulations of kindling-prone and kindling-resistant rats were found in both Wistar and WAG/Rij strains. Despite identical seizure responses to the first sound stimulation, AK progression dramatically differed between the two subpopulations. AK-prone rats exhibited rapid kindling development up to maximal stage-5 severity. In AK-resistant rats, limbic clonus did not appear after 30 stimulations or if it appeared, it did not progress beyond stage 2. The proportions of AK-prone and AK-resistant animals within Wistar and WAG/Rij strains were similar. Comparison of Wistar and WAG/Rij rats within the kindlingprone and kindling-resistant groups did not reveal a significant strain effect on AK progression. However, within the WAG/Rij strain, a significantly higher incidence of absence seizures was found in AK-resistant rats compared to AK-prone rats. Conclusions: The present study demonstrates that sensitivity to sound-induced epileptogenesis differs dramatically within Wistar and WAG/Rij strains, whereas genetic susceptibility to absence seizures does not change AK progression significantly. It is supposed that an increased incidence of nonconvulsive seizures and resistance to kindling result from a common seizure modulating mechanism.

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Section: Discussionmentioning

confidence: 99%

Audiogenic kindling in Wistar and WAG/Rij rats: Kindling‐prone and kindling‐resistant subpopulations

Vinogradova

2008

Epilepsia

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“…Amygdala kindling mimics the crucial phenotype of epilepsy: a chronically lowered seizure threshold (Ng et al, 2006). Amygdala kindled seizures evoke the typical behavioral manifestations of temporal lobe epilepsy (i.e., complex partial seizure or limbic motor seizure, in the rat) including behavior arrest, facial automatisms, and clonus (Sato et al, 1990).…”

Section: Introductionmentioning

confidence: 99%

Chemogenetic silencing of the midline and intralaminar thalamus blocks amygdala-kindled seizures

Wicker

Forcelli

2016

Experimental Neurology

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Temporal lobe epilepsy is the most common form of medically-intractable epilepsy. While seizures in TLE originate in structures such as hippocampus, amygdala, and temporal cortex, they propagate through a crucial relay: the midline/intralaminar thalamus. Prior studies have shown that pharmacological inhibition of midline thalamus attenuates limbic seizures. Here, we examined a recently developed technology, Designer Receptors Exclusively Activated by Designer Drugs (DREADDs), as a means of chemogenetic silencing to attenuate limbic seizures. Adult, male rats were electrically kindled from the amygdala, and injected with virus coding for inhibitory (hM4Di) DREADDs into the midline/intralaminar thalamus. When treated with the otherwise inert ligand Clozapine-N-Oxide (CNO) at doses of 2.5, 5, and 10 mg/kg, electrographic and behavioral seizure manifestations were suppressed in comparison to vehicle. At higher doses, we found complete blockade of seizure activity in a subset of subjects. CNO displayed a sharp time-response profile, with significant seizure attenuation seen 20-30 mins post injection, in comparison to 10 and 40 mins post injection. Seizures in animals injected with a control vector (i.e., no DREADD) were unaffected by CNO administration. These data underscore the crucial role of the midline/intralaminar thalamus in the propagation of seizures, specifically in the amygdala kindling model, and provide validation of chemogenetic silencing of limbic seizures.

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“…The gradual reduction of ADT was described earlier [23] and it may be related to histological [24], neurochemical [25] changes or to microhemorrhages and the deposition of iron [26]. The gradual reduction of the level of ADT can actually be observed as a consequence of the electrode implantation, but this was observed only after longer periods [23,27].…”

Section: Discussionmentioning

confidence: 92%

Cortical epileptogenesis of slowly kindled freely moving rats

Orbán-Kis

Száva

Szilágyi

2014

Acta Medica Marisiensis

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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.

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Afterdischarge threshold reduction in the kindling model of epilepsy

Cited by 11 publications

References 19 publications

Audiogenic kindling in Wistar and WAG/Rij rats: Kindling‐prone and kindling‐resistant subpopulations

Audiogenic kindling in Wistar and WAG/Rij rats: Kindling‐prone and kindling‐resistant subpopulations

Chemogenetic silencing of the midline and intralaminar thalamus blocks amygdala-kindled seizures

Cortical epileptogenesis of slowly kindled freely moving rats

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