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Epilepsia, ISSN 0013-9580, 07/2018, Volume 59, Issue 7, pp. 1455 - 1468
Summary Objective Na+/K+‐ATPase dysfunction, primary (mutation) or secondary (energy crisis, neurodegenerative disease) increases neuronal excitability in the... 
epilepsy | D801N | ATP1A3 | alternating hemiplegia of childhood | parvalbumin | ALTERNATING HEMIPLEGIA | DYSTONIA-PARKINSONISM | STRATUM-ORIENS | SPREADING DEPRESSION | CLINICAL NEUROLOGY | DE-NOVO MUTATIONS | SODIUM-PUMP | CA1 REGION | RAT HIPPOCAMPUS | RAPID-ONSET | FOCAL EPILEPSY | Interneurons - physiology | Sodium-Potassium-Exchanging ATPase - genetics | Sodium-Potassium-Exchanging ATPase - physiology | Humans | Evoked Potentials | Electroencephalography | Epilepsy - physiopathology | Mice, Neurologic Mutants | gamma-Aminobutyric Acid - physiology | Patch-Clamp Techniques | Animals | DNA Mutational Analysis | Hemiplegia - genetics | Pyramidal Cells - physiology | Epilepsy - genetics | Mice | Hemiplegia - physiopathology | In Vitro Techniques | Child | Hippocampus - physiopathology | Genetic Carrier Screening | Disease Models, Animal | Immunohistochemistry | Nervous system diseases | Neurons | Analysis | Epilepsy | GABA | Paralysis | Adenosine triphosphatase | Phenotypes | Interneurons | EEG | Brain slice preparation | Excitability | Action potential | Na+/K+-exchanging ATPase | Parvalbumin | Electrical stimuli | Depolarization | γ-Aminobutyric acid | Excitatory postsynaptic potentials | Pyramidal cells | Rodents | Hemiplegia | Glutamatergic transmission | Children | Mutation | Hippocampus | Bicuculline | Inhibitory postsynaptic potentials
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