ArticleEpilepsia2016
Bumetanide reduces seizure progression and the development of pharmacoresistant status epilepticus.
Article in Epilepsia, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.
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Who cites it
34 citing papers in PubMed, 70 citations in OpenAlex.
- Advancing the Paradigm of Temporal Lobe Epilepsy as a Network Disease: The Promise of Biomarkers and Targeted Disease Modification.International journal of molecular sciences · 2026Review
- WNK-SPAK/OSR1 signaling pathway facilitates ictal activity via reduced neuronal chloride extrusion rate.bioRxiv : the preprint server for biology · 2026Article
- GABACellular and molecular neurobiology · 2026Review
- Plasma KCC2, NKCC1, and GABA as peripheral biomarkers in autism spectrum disorder: a combined ROC analysis.Metabolic brain disease · 2026Article
- An Evaluation of Cation-Chloride Cotransporters NKCC1 and KCC2 in Carbamazepine-Resistant Rats.International journal of molecular sciences · 2025Article
- The NKCC1 Inhibitor Bumetanide Restores Cortical Feedforward Inhibition and Lessens Sensory Hypersensitivity in Early Postnatal Fragile X Mice.Biological psychiatry · 2025Article
- A drug repurposing screen reveals dopamine signaling as a critical pathway underlying potential therapeutics for the rare disease DPAGT1-CDG.PLoS genetics · 2024Article
- Evaluation of the Choroid Plexus Epithelium Inflammation TLR4/NF-κB/NKCC1 Signal Pathway Activation in the Development of Hydrocephalus.CNS neuroscience & therapeutics · 2024Article
- Ion transporter cascade, reactive astrogliosis and cerebrovascular diseases.Frontiers in pharmacology · 2024Review
- Treating Hyperexcitability in Human Cerebral Organoids Resulting from Oxygen-Glucose Deprivation.Cells · 2023Article
- Semaphorin 4D induced inhibitory synaptogenesis decreases epileptiform activity and alters progression to Status Epilepticus in mice.Epilepsy research · 2023Article
- Article
- Conditional deletion of KCC2 impairs synaptic plasticity and both spatial and nonspatial memory.Frontiers in molecular neuroscience · 2023Article
- Why won't it stop? The dynamics of benzodiazepine resistance in status epilepticus.Nature reviews. Neurology · 2022Review
- Experimental and real-world evidence supporting the computational repurposing of bumetanide forNature aging · 2021Article
- The Alteration of Chloride Homeostasis/GABAergic Signaling in Brain Disorders: Could Oxidative Stress Play a Role?Antioxidants (Basel, Switzerland) · 2021Review
- Preventing neuronal edema increases network excitability after traumatic brain injury.The Journal of clinical investigation · 2020Article
- The adenosine A1 receptor agonist WAG 994 suppresses acute kainic acid-induced status epilepticus in vivo.Neuropharmacology · 2020Article
- Screening for Efficacious Anticonvulsants and Neuroprotectants in Delayed Treatment Models of Organophosphate-induced Status Epilepticus.Neuroscience · 2020Article
- Biophysical Modeling Suggests Optimal Drug Combinations for Improving the Efficacy of GABA Agonists after Traumatic Brain Injuries.Journal of neurotrauma · 2019Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 2 countries.
Funding
Abstract
objectiveWe investigated the role of chloride homeostasis in seizure progression and development of pharmacoresistant status epilepticus (SE) by pharmacologically targeting the Na-K-Cl cotransporter (NKCC1) with bumetanide. We also investigated the ability of bumetanide to restore the efficacy of diazepam following SE.
methodsKainic acid (KA)-induced SE in vivo and 0-Mg(2+) -induced seizure-like events (SLEs) in vitro were monitored using electroencephalography (EEG) recordings in freely moving adult male mice and extracellular field potential recordings in acute entorhinal cortex-hippocampus slices, respectively. The ability of bumetanide to decrease epileptiform activity and prevent the development of pharmacoresistance to diazepam following SE was evaluated.
resultsBumetanide treatment significantly reduced KA-induced ictal activity in vivo and SLEs in vitro. In addition, bumetanide restored the efficacy of diazepam in decreasing ictal activity following SE in both the in vivo and in vitro models. SIGNIFICANCE: Our data demonstrate an anticonvulsant effect of bumetanide on KA-induced seizures in adult mice, suggesting a role for chloride plasticity in seizure progression. These data also demonstrate that the erosion of inhibition during seizure progression could underlie the development of pharmacoresistant SE and implicate a role for chloride plasticity in this process.
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Registered trials
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.