ArticleeNeuro
What Elements of the Inflammatory System Are Necessary for Epileptogenesis In Vitro?
Article in eNeuro. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
What it found
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Who cites it
6 citing papers in PubMed.
- A Dynamic Balance between Neuronal Death and Clearance in anThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2023Article
- Microglia attenuate the kainic acid-induced death of hippocampal neurons in slice cultures.Neuropsychopharmacology reports · 2020Article
- Epilepsy-on-a-Chip System for Antiepileptic Drug Discovery.IEEE transactions on bio-medical engineering · 2019Article
- Intrinsic Inflammation Is a Potential Anti-Epileptogenic Target in the Organotypic Hippocampal Slice Model.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2018Article
- Disruption of the ATP/adenosine balance in CD39Immunology · 2017Article
- Epileptogenesis in organotypic hippocampal cultures has limited dependence on culture medium composition.PloS one · 2017Article
Corrections and comments
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Authors and funding
4 authors.
Funding
Abstract
Epileptogenesis in vivo can be altered by manipulation of molecules such as cytokines and complement that subserve intercellular signaling in both the inflammatory and central nervous systems. Because of the dual roles of these signaling molecules, it has been difficult to precisely define the role of systemic inflammation in epileptogenesis. Organotypic hippocampal brain slices can be maintained in culture independently of the systemic inflammatory system, and the rapid course of epileptogenesis in these cultures supports the idea that inflammation is not necessary for epilepsy. However, this preparation still retains key cellular inflammatory mediators. Here, we found that rodent hippocampal organotypic slice cultures depleted of T lymphocytes and microglia developed epileptic activity at essentially the same rate and to similar degrees of severity as matched control slice cultures. These data support the idea that although the inflammatory system, neurons, and glia share key intercellular signaling molecules, neither systemic nor CNS-specific cellular elements of the immune and inflammatory systems are necessary components of epileptogenesis.
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Registered trials
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