ArticleAnnals of clinical and translational neurology2016
Rapamycin prevents acute dendritic injury following seizures.
Article in Annals of clinical and translational neurology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 11 citations in OpenAlex.
- Role of hippocampus in epileptogenesis: new insights in the cross-talks between the underlying mechanisms.Acta neurologica Belgica · 2025Review
- JC124 confers multimodal neuroprotection in epilepsy by suppressing NLRP3 inflammasome activation: evidence from animal and human neuronal models.Cell communication and signaling : CCS · 2025Article
- Article
- Glioma-Induced Alterations in Excitatory Neurons are Reversed by mTOR Inhibition.bioRxiv : the preprint server for biology · 2024Article
- The role of dendritic spines in epileptogenesis.Frontiers in cellular neuroscience · 2023Review
- Microglia provide structural resolution to injured dendrites after severe seizures.Cell reports · 2021Article
- Early treatment with C1 esterase inhibitor improves weight but not memory deficits in a rat model of status epilepticus.Physiology & behavior · 2019Article
- Wnt/β-catenin signaling as a potential target for novel epilepsy therapies.Epilepsy research · 2018Review
- Rapamycin Attenuates Acute Seizure-induced Astrocyte Injury in Mice in Vivo.Scientific reports · 2017Article
- Exploring Dendritic and Spine Structural Profiles in Epilepsy: Insights From Human Studies and Experimental Animal Models.Epilepsy currentsArticle
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
Abstract
objectiveSeizures cause acute structural changes in dendrites, which may contribute to cognitive deficits that occur in epilepsy patients. Disruption of the actin cytoskeleton of dendrites likely mediates the structural changes following seizures, but the upstream signaling mechanisms activated by synchronized physiological activity to cause seizure-induced dendritic injury are not known. In this study, we test the hypothesis that the mechanistic target of rapamycin complex 1 (mTORC1) pathway triggers structural changes in dendrites in response to seizures.
methodsIn vivo multiphoton imaging was performed in transgenic mice expressing green fluorescent protein in cortical neurons. The effect of rapamycin pre- and posttreatment was tested on kainate-induced dendritic injury and cofilin-mediated actin depolymerization.
resultsKainate-induced seizures caused acute activation of mTORC1 activity, which was prevented by the mTORC1 inhibitor, rapamycin. Rapamycin pretreatment, and to a lesser degree, posttreatment attenuated acute seizure-induced dendritic injury and correspondingly decreased LIM kinase and cofilin-mediated depolymerization of actin.
interpretationThe mTORC1 pathway mediates seizure-induced dendritic injury via depolymerization of actin. These findings have important mechanistic and translational applications for management of seizure-induced brain injury.
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Registered trials
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