ArticleProceedings of the National Academy of Sciences of the United States of America2001
Mice transgenically overexpressing sulfonylurea receptor 1 in forebrain resist seizure induction and excitotoxic neuron death.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 97 citations in OpenAlex.
- Transient Neonatal Diabetes Mellitus and Seizure with an Unknown Etiology.Journal of pediatric genetics · 2023Article
- The modulation of potassium channels by estrogens facilitates neuroprotection.Frontiers in cell and developmental biology · 2022Review
- Role of Modulation of Hippocampal Glucose Following Pilocarpine-Induced Status Epilepticus.Molecular neurobiology · 2021Article
- Analysis of KThe Malaysian journal of medical sciences : MJMS · 2021Article
- Structural Determinants of Insulin Release: Disordered N-Terminal Tail of Kir6.2 Affects Potassium Channel Dynamics through Interactions with Sulfonylurea Binding Region in a SUR1 Partner.The journal of physical chemistry. B · 2020Article
- Metabolic etiologies in West syndrome.Epilepsia open · 2018Review
- Potassium Channels and Human Epileptic Phenotypes: An Updated Overview.Frontiers in cellular neuroscience · 2016Review
- Optical control of insulin release using a photoswitchable sulfonylurea.Nature communications · 2014Article
- KATP channels modulate intrinsic firing activity of immature entorhinal cortex layer III neurons.Frontiers in cellular neuroscience · 2014Article
- Single KATP channel opening in response to stimulation of AMPA/kainate receptors is mediated by Na+ accumulation and submembrane ATP and ADP changes.The Journal of physiology · 2013Article
- The antiepileptic effect of the glycolytic inhibitor 2-deoxy-D-glucose is mediated by upregulation of K(ATP) channel subunits Kir6.1 and Kir6.2.Neurochemical research · 2013Article
- Neuroprotective role of ATP-sensitive potassium channels in cerebral ischemia.Acta pharmacologica Sinica · 2013Review
- Anticonvulsant effect of Diazoxide against Dichlorvos-induced seizures in mice.TheScientificWorldJournal · 2013Article
- Elevated expression of TDP-43 in the forebrain of mice is sufficient to cause neurological and pathological phenotypes mimicking FTLD-U.The Journal of experimental medicine · 2010Article
- Diazoxide reduces status epilepticus neuron damage in diabetes.Neurotoxicity research · 2010Article
- Noble gas xenon is a novel adenosine triphosphate-sensitive potassium channel opener.Anesthesiology · 2010Article
- Role of microglial IKKbeta in kainic acid-induced hippocampal neuronal cell death.Brain : a journal of neurology · 2008Article
- Metabolic environment in substantia nigra reticulata is critical for the expression and control of hypoglycemia-induced seizures.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2008Article
- How ATP inhibits the open K(ATP) channel.The Journal of general physiology · 2008Article
- Morphological localisation of sulfonylurea receptor 1 in endocrine cells of human, mouse and rat pancreas.Diabetologia · 2007Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
The ability of the sulfonylurea receptor (SUR) 1 to suppress seizures and excitotoxic neuron damage was assessed in mice transgenically overexpressing this receptor. Fertilized eggs from FVB mice were injected with a construct containing SUR cDNA and a calcium-calmodulin kinase IIalpha promoter. The resulting mice showed normal gross anatomy, brain morphology and histology, and locomotor and cognitive behavior. However, they overexpressed the SUR1 transgene, yielding a 9- to 12-fold increase in the density of [(3)H]glibenclamide binding to the cortex, hippocampus, and striatum. These mice resisted kainic acid-induced seizures, showing a 36% decrease in average maximum seizure intensity and a 75% survival rate at a dose that killed 53% of the wild-type mice. Kainic acid-treated transgenic mice showed no significant loss of hippocampal pyramidal neurons or expression of heat shock protein 70, whereas wild-type mice lost 68-79% of pyramidal neurons in the CA1-3 subfields and expressed high levels of heat shock protein 70 after kainate administration. These results indicate that the transgenic overexpression of SUR1 alone in forebrain structures significantly protects mice from seizures and neuronal damage without interfering with locomotor or cognitive function.
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