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            <funder>his work was supported by the Institut National de la Santé et de la Recherche Médicale (INSERM), and the National Centre for Scientific Research (CNRS). Funding sources had no involvement in the study design, collection, analysis, or interpretation of data, nor in the decision to publish.</funder>
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            <note type="commentary">This article contains several videos, here are the links.Supplementary Video S1: (Accessed on 10 April 2024, Link: https://urlz.fr/iPxZ). Supplementary Video S2: (Accessed on 10 April 2024, Link: https://urlz.fr/iPxP). (Supplementary Video S3, (Accessed on 10 April 2024, Link: https://urlz.fr/iOIz). (Supplementary Video S4, (Accessed on 10 April 2024, Link: https://urlz.fr/iOIA).(Supplementary Video S5, (Accessed on 10 April 2024, Link: https://urlz.fr/jlSX), (Supplementary Video S6, (Accessed on 10 April 2024, Link: https://urlz.fr/jlT1). Supplementary Video S7, (Accessed on 10 April 2024, Link: https://urlz.fr/jlTa). Supplementary Video S8, (Accessed on 10 April 2024, Link: https://urlz.fr/jlTr).</note>
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              <p>It has been known for a long time that epileptic seizures provoke brain neuroinflammation involving the activation of microglial cells. However, the role of these cells in this disease context and the consequences of their inflammatory activation on subsequent neuron network activity remain poorly understood so far. To fill this gap of knowledge and gain a better understanding of the role of microglia in the pathophysiology of epilepsy, we used an established zebrafish Dravet syndrome epilepsy model based on Scn1Lab sodium channel loss-of-function, combined with live microglia and neuronal Ca2+ imaging, local field potential (LFP) recording, and genetic microglia ablation. Data showed that microglial cells in scn1Lab-deficient larvae experiencing epileptiform seizures displayed morphological and biochemical changes characteristic of M1-like pro-inflammatory activation; i.e., reduced branching, amoeboid-like morphology, and marked increase in the number of microglia expressing pro-inflammatory cytokine Il1β. More importantly, LFP recording, Ca2+ imaging, and swimming behavior analysis showed that microglia-depleted scn1Lab-KD larvae displayed an increase in epileptiform seizure-like neuron activation when compared to that seen in scn1Lab-KD individuals with microglia. These findings strongly suggest that despite microglia activation and the synthesis of pro-inflammatory cytokines, these cells provide neuroprotective activities to epileptic neuronal networks, making these cells a promising therapeutic target in epilepsy.</p>
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              <p>On sait depuis longtemps que les crises d'épilepsie provoquent une neuroinflammation cérébrale impliquant l'activation des cellules microgliales. Cependant, le rôle de ces cellules dans ce contexte pathologique et les conséquences de leur activation inflammatoire sur l'activité ultérieure du réseau neuronal restent mal compris jusqu'à présent. Pour combler cette lacune et mieux comprendre le rôle de la microglie dans la physiopathologie de l'épilepsie, nous avons utilisé un modèle d'épilepsie du syndrome de Dravet chez le poisson zèbre basé sur la perte de fonction du canal sodique Scn1Lab, combiné à l'imagerie en direct de la microglie et du Ca2+ neuronal, à l'enregistrement du potentiel local de champ (LFP) et à l'ablation génétique de la microglie. Les données ont montré que les cellules microgliales des larves déficientes en scn1Lab présentant des crises épileptiformes présentaient des changements morphologiques et biochimiques caractéristiques d'une activation pro-inflammatoire de type M1, c'est-à-dire une ramification réduite, une morphologie de type amiboïde et une augmentation marquée du nombre de microglies exprimant la cytokine pro-inflammatoire Il1β. Plus important encore, l'enregistrement LFP, l'imagerie Ca2+ et l'analyse du comportement de nage ont montré que les larves scn1Lab-KD dépourvues de microglie présentaient une augmentation de l'activation des neurones épileptiformes semblables à des crises d'épilepsie par rapport à celle observée chez les individus scn1Lab-KD dotés de microglie. Ces résultats suggèrent fortement qu'en dépit de l'activation de la microglie et de la synthèse de cytokines pro-inflammatoires, ces cellules fournissent des activités neuroprotectrices aux réseaux neuronaux épileptiques, ce qui fait de ces cellules une cible thérapeutique prometteuse dans l'épilepsie.</p>
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