The role of basal ganglia in the control of generalized absence seizures

Deransart, Colin; Vercueil, Laurent; Marescaux, C.; Depaulis, Antoine

doi:10.1016/s0920-1211(98)00053-9

Cited by 151 publications

(116 citation statements)

References 77 publications

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“…Two structures will be mentioned here: the substantia nigra pars reticulata (SNr), where several pharmacological manipulations as well as electrical stimulation have been shown to modulate SWD activity (Deransart et al, 1998;Feddersen et al, 2007). Also, drug injection into the hippocampus modulates SWDs (Tolmacheva and van Luijtelaar, 2007).…”

Section: Brain Regions Of Interestmentioning

confidence: 99%

Upholding WAG/Rij rats as a model of absence epileptogenesis: Hidden mechanisms and a new theory on seizure development

Russo

Citraro

Constanti³

et al. 2016

Neuroscience & Biobehavioral Reviews

128

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Upholding WAG/Rij rats as a model of absence epileptogenesis: Hidden mechanisms and a new theory on seizure development.Neuroscience and Biobehavioral Reviews http://dx.doi.org/10. 1016/j.neubiorev.2016.09.017 This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain. AbstractThe WAG/Rij rat model has recently gathered attention as a suitable animal model of absence epileptogenesis. This latter term has a broad definition encompassing any possible cause that determines the development of spontaneous seizures; however, most of, if not all, preclinical knowledge on epileptogenesis is confined to the study of post-brain insult models such as traumatic brain injury or post-status epilepticus models. WAG/Rij rats, but also synapsin 2 knockout, Kv7 current-deficient mice represent the first examples of genetic models where an efficacious antiepileptogenic treatment (ethosuximide) was started before seizure onset. In this review, we have critically reconsidered all articles published regarding WAG/Rij rats, from the perspective that the period before SWD onset is considered as the latent period. In our new theory on seizure development, it is proposed that genes might be considered as the initial "insult" responsible for all plastic changes underpinning the development of spontaneous seizures. According to this idea, in WAG/Rij rats, genetic predisposition would lead to the development of abnormal bilateral cortical epileptic foci, which would then nongenetically stimulate the rest of the brain to rearrange networks in order to phenotypically develop seizures similarly to what happens during electrical kindling.

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Section: Brain Regions Of Interestmentioning

confidence: 99%

Upholding WAG/Rij rats as a model of absence epileptogenesis: Hidden mechanisms and a new theory on seizure development

Russo

Citraro

Constanti³

et al. 2016

Neuroscience & Biobehavioral Reviews

128

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“…Finally, the inhibitory effect by the Seizure activities induced by the excitatory input from SRN to TRN Until now, it is shown that there are three main arguments about origin of the epileptic seizures: (1) SWDs generated in cortex neurons; (2) SWDs generated in thalamus neurons; (3) SWDs appeared in cortex neurons, and it transforms from a ''spindles'' wave generated in thalamus neurons (Breakspear et al 2006). Hence, the thalamus neurons can play a vital role in the generation of epileptic seizures (Breakspear et al 2006;Deransart et al 1998;Paz et al 2007). Thus, theoretical exploration about this from the modeling should be conducted to well understand the generation of epileptic seizures.…”

Section: Seizure Activities Induced By the Pathway From Srn To Excitamentioning

confidence: 99%

“…And, many experimental data show that variation of the firing rates in SNr can greatly affect seizure activity in corticothalamic circuit (Deransart et al 1998;Kase et al 2012). The effect of outputs in SNr on the firing activity of corticothalamic circuit can directly project to TRN or SRN (Gulcebi et al 2012), or from the SNr to thalamic reticular nucleus relaying at SRN by the indirect pathway (Deransart et al 1998). In particular, main question involved in the present study is how to control SWDs in the corticothalamic system with changing projection strength of different pathways.…”

Section: Introductionmentioning

confidence: 99%

Control of absence seizures induced by the pathways connected to SRN in corticothalamic system

Guo

Wang

2014

Cogn Neurodyn

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The cerebral cortex, thalamus and basal ganglia together form an important network in the brain, which is closely related to several nerve diseases, such as parkinson disease, epilepsy seizure and so on. Absence seizure can be characterized by 2-4 Hz oscillatory activity, and it can be induced by abnormal interactions between the cerebral cortex and thalamus. Many experimental results have also shown that basal ganglia are a key neural structure, which closely links the corticothalamic system in the brain. Presently, we use a corticothalamic-basal ganglia model to study which pathways in corticothalamic system can induce absence seizures and how these oscillatory activities can be controlled by projections from the substantia nigra pars reticulata (SNr) to the thalamic reticular nucleus (TRN) or the specific relay nuclei (SRN) of the thalamus. By tuning the projection strength of the pathway ''Excitatory pyramidal cortex-SRN'', ''SRN-Excitatory pyramidal cortex'' and ''SRN-TRN'' respectively, different firing states including absence seizures can appear. This indicates that absence seizures can be induced by tuning the connection strength of the considered pathway. In addition, typical absence epilepsy seizure state ''spike-and-slow wave discharges'' can be controlled by adjusting the activation level of the SNr as the pathways SNr-SRN and SNr-TRN open independently or together. Our results emphasize the importance of basal ganglia in controlling absence seizures in the corticothalamic system, and can provide a potential idea for the clinical treatment.

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“…Recent pharmacological studies performed in genetic absence epilepsy rats from Strasbourg (GAERS), a well established genetic model of absence epilepsy (Marescaux et al, 1992;Danober et al, 1998), indicate that the basal ganglia circuits could act as a remote control system for absence seizures via a modulation of activity in the striatonigral pathway (Depaulis et al, 1988(Depaulis et al, , 1989Danober et al, 1998;Deransart et al, 1998Deransart et al, , 2000Deransart et al, , 2001Deransart and Depaulis, 2002). Specifically, the frequency of absence seizures is significantly decreased by injection of GABA A receptor agonists into the substantia nigra pars reticulata (SNr) or by the activation of GABAergic striatonigral neurons after intrastriatal injection of NMDA or dopaminergic D 1 receptor agonists (Depaulis et al, 1988;Deransart et al, 1998).…”

Section: Introductionmentioning

confidence: 99%

“…Specifically, the frequency of absence seizures is significantly decreased by injection of GABA A receptor agonists into the substantia nigra pars reticulata (SNr) or by the activation of GABAergic striatonigral neurons after intrastriatal injection of NMDA or dopaminergic D 1 receptor agonists (Depaulis et al, 1988;Deransart et al, 1998). Conversely, the pharmacological blockade of GABA A receptors in the SNr or the blockade of striatal D 1 receptors aggravates absence seizures (Deransart et al, 2000(Deransart et al, , 2001.…”

Section: Introductionmentioning

confidence: 99%

On the Activity of the Corticostriatal Networks during Spike-and-Wave Discharges in a Genetic Model of Absence Epilepsy

Slaght¹,

Paz²,

Chávez³

et al. 2004

J. Neurosci.

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Absence seizures are characterized by impairment of consciousness associated with widespread bilaterally synchronous spike-and-wave discharges (SWDs) in the electroencephalogram (EEG), which reflect highly synchronized oscillations in thalamocortical networks. Although recent pharmacological studies suggest that the basal ganglia could provide a remote control system for absence seizures, the mechanisms of propagation of epileptic discharges in these subcortical nuclei remain unknown. In the present study, we provide the first description of the electrical events in the corticostriatal pathway during spontaneous SWDs in the genetic absence epilepsy rats from Strasbourg (GAERS), a genetic model of absence epilepsy. In corticostriatal neurons, the SWDs were associated with suprathreshold rhythmic depolarizations in-phase with local EEG spikes. Consistent with this synchronized firing in their excitatory cortical afferents, striatal output neurons (SONs) exhibited, during SWDs, large-amplitude rhythmic synaptic depolarizations. However, SONs did not discharge during SWDs. Instead, the rhythmic synaptic excitation of SONs was shunted by a Cl Ϫ -dependent increase in membrane conductance that was temporally correlated with bursts of action potentials in striatal GABAergic interneurons. The reduced SON excitability accompanying absence seizures may participate in the control of SWDs by affecting the flow of cortical information within the basal ganglia circuits.

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The role of basal ganglia in the control of generalized absence seizures

Cited by 151 publications

References 77 publications

Upholding WAG/Rij rats as a model of absence epileptogenesis: Hidden mechanisms and a new theory on seizure development

Upholding WAG/Rij rats as a model of absence epileptogenesis: Hidden mechanisms and a new theory on seizure development

Control of absence seizures induced by the pathways connected to SRN in corticothalamic system

On the Activity of the Corticostriatal Networks during Spike-and-Wave Discharges in a Genetic Model of Absence Epilepsy

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