ArticleNature medicine2015
Treatment during a vulnerable developmental period rescues a genetic epilepsy.
Article in Nature medicine, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 59 papers.
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Who cites it
59 citing papers in PubMed, 124 citations in OpenAlex.
- Clarifications regarding bumetanide for neonatal seizures.Epilepsia · 2022Trial
- Prevention of Epilepsy in Infants with Tuberous Sclerosis Complex in the EPISTOP Trial.Annals of neurology · 2021Trial
- Reversibility and therapeutic feasibility of DNM1L-associated neurodevelopmental disorders.Experimental & molecular medicine · 2026Article
- Early and transient increase in cortical pyramidal cell excitability and delayed alteration of evoked synaptic transmission and t-SNARE proteins content in the hippocampus and neocortex of neonatal and juvenileFrontiers in cellular neuroscience · 2026Article
- Transgenic mouse models of sodium and potassium channelopathies in epilepsy: insights into disease mechanisms and therapeutics.Bioscience reports · 2025Review
- Prediction of Pharmacoresistance in Drug-Naïve Temporal Lobe Epilepsy Using Ictal EEGs Based on Convolutional Neural Network.Neuroscience bulletin · 2025Article
- Limitations of genomics to predict and treat autism: a disorder born in the womb.Journal of medical genetics · 2025Review
- Gene-replacement therapy in neurodevelopmental disorders: progress and challenges.The Journal of clinical investigation · 2025Review
- Network state transitions during cortical development.Nature reviews. Neuroscience · 2024Review
- Reelin Regulates Developmental Desynchronization Transition of Neocortical Network Activity.Biomolecules · 2024Article
- Synchronous excitation in the superficial and deep layers of the medial entorhinal cortex precedes early sharp waves in the neonatal rat hippocampus.Frontiers in cellular neuroscience · 2024Article
- The human channel gating-modifying A749G CACNA1D (Cav1.3) variant induces a neurodevelopmental syndrome-like phenotype in mice.JCI insight · 2023Article
- Somatosensory-Evoked Early Sharp Waves in the Neonatal Rat Hippocampus.International journal of molecular sciences · 2023Article
- The long-term effects of maternal deprivation on the number and size of inhibitory interneurons in the rat amygdala and nucleus accumbens.Frontiers in neuroscience · 2023Article
- Neuronal splicing regulator RBFOX3 mediates seizures via regulatingProceedings of the National Academy of Sciences of the United States of America · 2022Article
- Severe inflammation in new-borns induces long-term cognitive impairment by activation of IL-1β/KCC2 signaling during early development.BMC medicine · 2022Article
- Article
- Bumetanide Effects on Resting-State EEG in Tuberous Sclerosis Complex in Relation to Clinical Outcome: An Open-Label Study.Frontiers in neuroscience · 2022Article
- Critical periods inFrontiers in physiology · 2022Review
- Spontaneous seizure and memory loss in mice expressing an epileptic encephalopathy variant in the calmodulin-binding domain of KProceedings of the National Academy of Sciences of the United States of America · 2021Article
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Authors and funding
11 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The nervous system is vulnerable to perturbations during specific developmental periods. Insults during such susceptible time windows can have long-term consequences, including the development of neurological diseases such as epilepsy. Here we report that a pharmacological intervention timed during a vulnerable neonatal period of cortical development prevents pathology in a genetic epilepsy model. By using mice with dysfunctional Kv7 voltage-gated K(+) channels, which are mutated in human neonatal epilepsy syndromes, we demonstrate the safety and efficacy of the sodium-potassium-chloride cotransporter NKCC1 antagonist bumetanide, which was administered during the first two postnatal weeks. In Kv7 current-deficient mice, which normally display epilepsy, hyperactivity and stereotypies as adults, transient bumetanide treatment normalized neonatal in vivo cortical network and hippocampal neuronal activity, prevented structural damage in the hippocampus and restored wild-type adult behavioral phenotypes. Furthermore, bumetanide treatment did not adversely affect control mice. These results suggest that in individuals with disease susceptibility, timing prophylactically safe interventions to specific windows during development may prevent or arrest disease progression.
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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.