Suppression of Absence Seizures by Electrical and Pharmacological Activation of the Caudal Superior Colliculus in a Genetic Model of Absence Epilepsy in the Rat

Nail-Boucherie, Karine; Lê-Pham, Bich-Thuy; Marescaux, Christian; Depaulis, Antoine

doi:10.1006/exnr.2002.7997

Cited by 24 publications

(22 citation statements)

References 47 publications

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“…This seizure suppression indicates a role for DLSC in regulating the initiation of these seizures, even though the site of initiation is distal to the SC (i.e., in the thalamus). This finding is consistent with reports of anti-seizure effects of collicular activation in genetically absence prone rats (A Depaulis et al, 1990a; Nail-Boucherie et al, 2002), as well as in evoked absence seizure models (Redgrave et al, 1988). …”

Section: Discussionsupporting

confidence: 93%

“…We observed a pronounced seizure-suppressive effect against thalamocortical spike-and-wave seizures, consistent with prior reports (A Depaulis et al, 1990a, 1990b; Nail-Boucherie et al, 2002; Redgrave et al, 1988). This seizure suppression indicates a role for DLSC in regulating the initiation of these seizures, even though the site of initiation is distal to the SC (i.e., in the thalamus).…”

Section: Discussionsupporting

confidence: 92%

“…We found that activation of DLSC at frequencies as low as 5 Hz was sufficient to suppress seizure activity. While one prior study has examined electrical activation of DLSC (25 Hz) against seizures in genetically absence epileptic rats from Strasbourg (Nail-Boucherie et al, 2002), electrical stimulation only produced a transient suppression of seizure activity (Nail-Boucherie et al, 2002). By comparison, our manipulation suppressed activity throughout the observation period, even at lower stimulation rates.…”

Section: Discussionmentioning

confidence: 99%

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Optogenetic activation of superior colliculus neurons suppresses seizures originating in diverse brain networks

Soper

Wicker

Kulick

et al. 2016

Neurobiology of Disease

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Because sites of seizure origin may be unknown or multifocal, identifying targets from which activation can suppress seizures originating in diverse networks is essential. We evaluated the ability of optogenetic activation of the deep/intermediate layers of the superior colliculus (DLSC) to fill this role. Optogenetic activation of DLSC suppressed behavioral and electrographic seizures in the pentylenetetrazole (forebrain+brainstem seizures) and Area Tempestas (forebrain/complex partial seizures) models; this effect was specific to activation of DLSC, and not neighboring structures. DLSC activation likewise attenuated seizures evoked by gamma butyrolactone (thalamocortical/absence seizures), or acoustic stimulation of genetically epilepsy prone rates (brainstem seizures). Anticonvulsant effects were seen with stimulation frequencies as low as 5 Hz. Unlike previous applications of optogenetics for the control of seizures, activation of DLSC exerted broad-spectrum anticonvulsant actions, attenuating seizures originating in diverse and distal brain networks. These data indicate that DLSC is a promising target for optogenetic control of epilepsy.

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Section: Discussionsupporting

confidence: 93%

Section: Discussionsupporting

confidence: 92%

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

Optogenetic activation of superior colliculus neurons suppresses seizures originating in diverse brain networks

Soper

Wicker

Kulick

et al. 2016

Neurobiology of Disease

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show abstract

“…They were implanted under general anesthesia [diazepam (DZP), 4 mg/kg + ketamine, 1,000 mg/kg, i.p.] with four single‐contact recording electrodes, as previously described (3). Stainless‐steel guide‐cannulae (o.d., 0.4 mm; i.d., 0.3 mm) were aimed bilaterally at (a) the deep layers of the caudal part of the SC (A/P, –7.3 mm; M/L, 2.0 mm; D/V, –4.0 mm from bregma), or (b) the Pf (A/P, –4.80 mm; M/L, 1.5 mm; D/V, 4.4 mm from bregma).…”

Section: Methodsmentioning

confidence: 99%

“…Recently we showed that the neuronal populations of the intermediate and superficial layers of the caudal superior colliculus (SC) may constitute an important relay for the control of absence seizures by the basal ganglia, via the SNR (3). One of the main outputs of the SC is the ascending projection to the centromedial and the parafascicular nuclei (Pf) of the thalamus, two main components of the intralaminar nuclei (4,5).…”

mentioning

confidence: 99%

Evidence for a Role of the Parafascicular Nucleus of the Thalamus in the Control of Epileptic Seizures by the Superior Colliculus

et al. 2005

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Summary:Purpose: The aim of this study was to investigate whether the nucleus parafascicularis (Pf) of the thalamus could be a relay of the control of epileptic seizures by the superior colliculus (SC). The Pf is one of the main ascending projections of the SC, the disinhibition of which has been shown to suppress seizures in different animal models and has been proposed as the main relay of the nigral control of epilepsy.Methods: Rats with genetic absence seizures (generalized absence epilepsy rat from Strasbourg or GAERS) were used in this study. The effect of bilateral microinjection of picrotoxin, a γ -aminobutyric acid (GABA) antagonist, in the SC on the glutamate and GABA extracellular concentration within the Pf was first investigated by using microdialysis. In a second experiment, the effect of direct activation of Pf neurons on the occurrence of absence seizures was examined with microinjection of low doses of kainate, a glutamate agonist.Results: Bilateral injection of picrotoxin (33 pmol/side) in the SC suppressed spike-and-wave discharges for 20 min. This treatment resulted in an increase of glutamate but not GABA levels in the Pf during the same time course. Bilateral injection of kainate (35 pmol/side) into the Pf significantly suppressed spike-and-wave discharges for 20 min, whereas such injections were without effects when at least one site was located outside the Pf.Conclusions: These data suggest that glutamatergic projections to the Pf could be involved in the control of seizures by the SC. Disinhibition of these neurons could lead to seizure suppression and may be involved in the nigral control of epilepsy.

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The role of the basal ganglia in the control of seizure

Vuong

Devergnas

2017

J Neural Transm

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Epilepsy is a network disorder and each type of seizure involves distinct cortical and subcortical network, differently implicated in the control and propagation of the ictal activity. The role of the basal ganglia has been revealed in several cases of focal and generalized seizures. Here, we review the data that show the implication of the basal ganglia in absence, temporal lobe, and neocortical seizures in animal models (rodent, cat, and non-human primate) and in human. Based on these results and the advancement of deep brain stimulation for Parkinson's disease, basal ganglia neuromodulation has been tested with some success that can be equally seen as promising or disappointing. The effect of deep brain stimulation can be considered promising with a 76% in seizure reduction in temporal lobe epilepsy patients, but also disappointing, since only few patients have become seizure free and the antiepileptic effects have been highly variable among patients. This variability could probably be explained by the heterogeneity among the patients included in these clinical studies. To illustrate the importance of specific network identification, electrophysiological activity of the putamen and caudate nucleus has been recorded during penicillin-induced pre-frontal and motor seizures in one monkey. While an increase of the firing rate was found in putamen and caudate nucleus during pre-frontal seizures, only the activity of the putamen cells was increased during motor seizures. These preliminary results demonstrate the implication of the basal ganglia in two types of neocortical seizures and the necessity of studying the network to identify the important nodes implicated in the propagation and control of each type of seizure.

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Suppression of Absence Seizures by Electrical and Pharmacological Activation of the Caudal Superior Colliculus in a Genetic Model of Absence Epilepsy in the Rat

Cited by 24 publications

References 47 publications

Optogenetic activation of superior colliculus neurons suppresses seizures originating in diverse brain networks

Optogenetic activation of superior colliculus neurons suppresses seizures originating in diverse brain networks

Evidence for a Role of the Parafascicular Nucleus of the Thalamus in the Control of Epileptic Seizures by the Superior Colliculus

The role of the basal ganglia in the control of seizure

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