ArticleProceedings of the National Academy of Sciences of the United States of America1995
Limbic epilepsy in transgenic mice carrying a Ca2+/calmodulin-dependent kinase II alpha-subunit mutation.
Article in Proceedings of the National Academy of Sciences of the United States of America, 1995. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
43 citing papers in PubMed, 135 citations in OpenAlex.
- Transcriptome profiling reveals major structural genes, transcription factors and biosynthetic pathways in refractory epilepsy in tropical region of China.BMC neurology · 2025Article
- The Traf2 and NcK interacting kinase inhibitor NCB-0846 suppresses seizure activity involving the decrease of GRIA1.Genes & diseases · 2024Article
- Behavioral and Molecular Responses to Exogenous Cannabinoids During Pentylenetetrazol-Induced Convulsions in Male and Female Rats.Frontiers in molecular neuroscience · 2022Article
- Role of CaFrontiers in molecular neuroscience · 2022Review
- Calcium/Calmodulin-Dependent Protein Kinase II in Cerebrovascular Diseases.Translational stroke research · 2021Review
- Amnesia for context fear is caused by widespread disruption of hippocampal activity.Neurobiology of learning and memory · 2020Article
- CAMK2-Dependent Signaling in Neurons Is Essential for Survival.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2019Article
- Transcriptomic immaturity inducible by neural hyperexcitation is shared by multiple neuropsychiatric disorders.Communications biology · 2019Article
- Voltage-Dependent Calcium Channels, Calcium Binding Proteins, and Their Interaction in the Pathological Process of Epilepsy.International journal of molecular sciences · 2018Review
- Everolimus is better than rapamycin in attenuating neuroinflammation in kainic acid-induced seizures.Journal of neuroinflammation · 2017Article
- Identifying and Analyzing Novel Epilepsy-Related Genes Using Random Walk with Restart Algorithm.BioMed research international · 2017Article
- mTOR and MAPK: from localized translation control to epilepsy.BMC neuroscience · 2016Review
- Neuronal calcium/calmodulin-dependent protein kinase II mediates nicotine reward in the conditioned place preference test in mice.Behavioural pharmacology · 2016Article
- The immature dentate gyrus represents a shared phenotype of mouse models of epilepsy and psychiatric disease.Bipolar disorders · 2013Article
- Article
- Phosphodiesterase-III Inhibitors Amrinone and Milrinone on Epilepsy and Cardiovascular Activities.North American journal of medical sciences · 2012Article
- Calcium/calmodulin-dependent protein kinase II (CaMKII) inhibition induces neurotoxicity via dysregulation of glutamate/calcium signaling and hyperexcitability.The Journal of biological chemistry · 2012Article
- α-Calcium calmodulin kinase II modulates the temporal structure of hippocampal bursting patterns.PloS one · 2012Article
- CaMKII in cerebral ischemia.Acta pharmacologica Sinica · 2011Review
- PTPBR7 binding proteins in myelinating neurons of the mouse brain.International journal of biological sciences · 2011Article
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
Abstract
Multifunctional Ca2+/calmodulin-dependent protein kinase II (CaMK) phosphorylates proteins pivotally involved in diverse neuronal processes and thereby coordinates cellular responses to external stimuli that regulate intracellular Ca2+ [Hanson, P. I. & Schulman, H. (1992) Annu. Rev. Biochem. 61, 559-664]. Despite extensive study, the impact of this enzyme on control of the excitability of neuron populations in the mammalian nervous system in situ is unknown. To address this question, we studied transgenic mice carrying a null mutation (-/-) for the alpha subunit of CaMK. In contrast to wild-type littermates, null mutants exhibit profound hyperexcitability, evident in epileptic seizures involving limbic structures including the hippocampus. No evidence of increased excitability was detected in mice carrying null mutations of the gamma isoform of protein kinase C, underscoring the specificity of the effect of CaMK. CaMK plays a powerful and previously underappreciated role in control of neuronal excitability in the mammalian nervous system. These insights have important implications for analyses of mechanisms of epilepsy and, perhaps, learning and memory.
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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.