ArticleNeurobiology of disease2012
Interictal spikes, seizures and ictal cell death are not necessary for post-traumatic epileptogenesis in vitro.
Article in Neurobiology of disease, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.
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Who cites it
44 citing papers in PubMed, 67 citations in OpenAlex.
- WNK-SPAK/OSR1 signaling pathway facilitates ictal activity via reduced neuronal chloride extrusion rate.bioRxiv : the preprint server for biology · 2026Article
- Cell-generated mechanical forces play a role in epileptogenesis after injury.Experimental neurology · 2025Article
- Chemogenetics with PSAMGene therapy · 2025Article
- Selective modulation of epileptic tissue by an adenosine ABritish journal of pharmacology · 2024Article
- The NLRP3 Inflammasome in Neurodegenerative Disorders: Insights from Epileptic Models.Biomedicines · 2023Review
- A Dynamic Balance between Neuronal Death and Clearance in anThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2023Article
- A genetically targeted ion sensor reveals distinct seizure-related chloride and pH dynamics in GABAergic interneuron populations.iScience · 2023Article
- Targeting firing rate neuronal homeostasis can prevent seizures.Disease models & mechanisms · 2022Article
- In vitro ictogenesis is stochastic at the single neuron level.Brain : a journal of neurology · 2022Article
- Disrupting Epileptiform Activity by Preventing Parvalbumin Interneuron Depolarization Block.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2021Article
- Variability of seizure-like activity in anHeliyon · 2020Article
- Neural layer self-assembly in geometrically confined rat and human 3D cultures.Biofabrication · 2019Article
- Kinase Inhibitors with Antiepileptic Properties Identified with a Novel in Vitro Screening Platform.International journal of molecular sciences · 2019Article
- Epilepsy-on-a-Chip System for Antiepileptic Drug Discovery.IEEE transactions on bio-medical engineering · 2019Article
- The Paroxysmal Depolarization Shift: Reconsidering Its Role in Epilepsy, Epileptogenesis and Beyond.International journal of molecular sciences · 2019Review
- A Proposed Mechanism for Spontaneous Transitions between Interictal and Ictal Activity.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2019Article
- How do we use in vitro models to understand epileptiform and ictal activity? A report of the TASK1-WG4 group of the ILAE/AES Joint Translational Task Force.Epilepsia open · 2018Article
- Transient ischemia facilitates neuronal chloride accumulation and severity of seizures.Annals of clinical and translational neurology · 2018Article
- Gabapentin Prevents Progressive Increases in Excitatory Connectivity and Epileptogenesis Following Neocortical Trauma.Cerebral cortex (New York, N.Y. : 1991) · 2018Article
- Ex vivo model of epilepsy in organotypic slices-a new tool for drug screening.Journal of neuroinflammation · 2018Article
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Authors and funding
4 authors at 2 institutions in 1 country.
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Abstract
Clinical studies indicate that phenytoin prevents acute post-traumatic seizures but not subsequent post-traumatic epilepsy. We explored this phenomenon using organotypic hippocampal slice cultures as a model of severe traumatic brain injury. Hippocampal slices were cultured for up to eight weeks, during which acute and chronic electrical recordings revealed a characteristic evolution of spontaneous epileptiform discharges, including interictal spikes, seizure activity and electrical status epilepticus. Cell death exhibited an early peak immediately following slicing, and a later secondary peak that coincided with the peak of seizure-like activity. The secondary peak in neuronal death was abolished by either blockade of glutamatergic transmission with kynurenic acid or by elimination of ictal activity and status epilepticus with phenytoin. Withdrawal of kynurenic acid or phenytoin was followed by a sharp increase in spontaneous seizure activity. Phenytoin's anticonvulsant and neuroprotective effects failed after four weeks of continuous administration. These data support the clinical findings that after brain injury, anticonvulsants prevent seizures but not epilepsy or the development of anticonvulsant resistance. We extend the clinical data by showing that secondary neuronal death is correlated with ictal but not interictal activity, and that blocking all three of these sequelae of brain injury does not prevent epileptogenesis in this in vitro model.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.