Associated Papers
Scn1a and Cacna1a mutations mutually alter their original phenotypes in rats.
Ohmori I et al.
Neurochemistry International, 2020
Establishment of isogenic iPSCs from an individual with SCN1A mutation mosaicism as a model for investigating neurocognitive impairment in Dravet syndrome.
Maeda H et al.
Journal of Human Genetics, 2016
Pathogenesis and new candidate treatments for infantile spasms and early life epileptic encephalopathies: A view from preclinical studies.
Galanopoulou AS et al.
Neurobiology of Disease, 2015
Advances on genetic rat models of epilepsy.
Serikawa T et al.
Experimental Animals, 2015
Methylphenidate improves learning impairments and hyperthermia-induced seizures caused by an Scn1a mutation.
Ohmori I et al.
Epilepsia, 2014
Febrile temperatures unmask biophysical defects in Nav1.1 epilepsy mutations supportive of seizure initiation.
Volkers L et al.
The Journal of General Physiology, 2013
Inhalation of 10% carbon dioxide rapidly terminates Scn1a mutation-related hyperthermia-induced seizures.
Ohmori I et al.
Epilepsy Research, 2013
High-frequency EEG oscillations in hyperthermia-induced seizures of Scn1a mutant rats.
Kobayashi K et al.
Epilepsy Research, 2013
Scn1a missense mutation causes limbic hyperexcitability and vulnerability to experimental febrile seizures.
Ohno Y et al.
Neurobiology of Disease, 2011
Scn1a missense mutation impairs GABAA receptor-mediated synaptic transmission in the rat hippocampus.
Ohno Y et al.
Biochemical and Biophysical Research Communications, 2010
A missense mutation of the gene encoding voltage-dependent sodium channel (Nav1.1) confers susceptibility to febrile seizures in rats.
Mashimo T et al.
The Journal of Neuroscience : the Official Journal of the Society for Neuroscience, 2010
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