ArticleBritish journal of pharmacology2008
Standard antiepileptic drugs fail to block epileptiform activity in rat organotypic hippocampal slice cultures.
Article in British journal of pharmacology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed.
- The microbiota-gut-brain axis and epilepsy from a multidisciplinary perspective: Clinical evidence and technological solutions for improvement of in vitro preclinical models.Bioengineering & translational medicine · 2022Review
- Excitatory GABAergic signalling is associated with benzodiazepine resistance in status epilepticus.Brain : a journal of neurology · 2019Article
- The 4-Aminopyridine Model of Acute SeizuresFrontiers in neuroscience · 2019Article
- NMDA-receptor inhibition and oxidative stress during hippocampal maturation differentially alter parvalbumin expression and gamma-band activity.Scientific reports · 2018Article
- Chemogenetic Recruitment of Specific Interneurons Suppresses Seizure Activity.Frontiers in cellular neuroscience · 2018Article
- The Subiculum: A Potential Site of Ictogenesis in a Neonatal Seizure Model.Frontiers in neurology · 2017Article
- DREADDs suppress seizure-like activity in a mouse model of pharmacoresistant epileptic brain tissue.Gene therapy · 2016Article
- Acid-sensing ion channels regulate spontaneous inhibitory activity in the hippocampus: possible implications for epilepsy.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2016Article
- How might novel technologies such as optogenetics lead to better treatments in epilepsy?Advances in experimental medicine and biology · 2014Review
- Issues related to development of new antiseizure treatments.Epilepsia · 2013Review
- Seizures as imbalanced up states: excitatory and inhibitory conductances during seizure-like events.Journal of neurophysiology · 2013Article
- Possible alterations in GABAA receptor signaling that underlie benzodiazepine-resistant seizures.Epilepsia · 2012Review
- Neuron to astrocyte communication via cannabinoid receptors is necessary for sustained epileptiform activity in rat hippocampus.PloS one · 2012Article
- Surface charge impact in low-magnesium model of seizure in rat hippocampus.Journal of neurophysiology · 2012Article
- Magnolol, a major bioactive constituent of the bark of Magnolia officinalis, exerts antiepileptic effects via the GABA/benzodiazepine receptor complex in mice.British journal of pharmacology · 2011Article
- An organotypic hippocampal slice culture model of excitotoxic injury induced spontaneous recurrent epileptiform discharges.Brain research · 2011Article
- Difficulties in Treatment and Management of Epilepsy and Challenges in New Drug Development.Pharmaceuticals (Basel, Switzerland) · 2010Review
- Optogenetic control of epileptiform activity.Proceedings of the National Academy of Sciences of the United States of America · 2009Article
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3 authors.
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Abstract
background and purposeEarlier studies had demonstrated that tonic-clonic seizure-like events (SLEs) resembling electrographic correlates of limbic seizures in animals and humans can be induced in organotypic hippocampal slice cultures (OHSCs). We have explored OHSCs for their suitability to serve as in vitro models of limbic seizures for studying seizure mechanisms and screening new antiepileptic compounds. EXPERIMENTAL APPROACH: OHSCs were cultivated according to the interface method. Neuronal activity and extracellular potassium concentration were recorded under submerged conditions. SLEs were induced by lowering magnesium concentration or by applying the potassium channel blocker 4-aminopyridine. The effects of standard antiepileptic drugs (AEDs), carbamazepine, phenytoin, valproic acid, clonazepam, diazepam and phenobarbital sodium on SLEs were analysed. KEY
resultsIn more than 93% of OHSCs, AEDs did not prevent the induction of SLEs or stop ongoing seizure activity even when toxic concentrations were applied. This pharmacoresistance was independent of the method of seizure provocation, postnatal age at explantation (P2-P10) and cultivation time in vitro (2 months). SLEs were reversibly blocked by glutamate antagonists or the GABA(A)-agonist muscimol. CONCLUSIONS AND IMPLICATIONS: We present a simple to establish in vitro model of tonic-clonic SLEs that is a priori pharmacoresistant and thus has an advantage over animal models of pharmacoresistant seizures in which responders and non-responders can be sorted out only after an experiment. OHSCs could be suitable for exploring mechanisms of pharmacoresistant seizures and be used for the identification of new anticonvulsive compounds eventually effective in drug refractory epilepsy.
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