about
Genetic epilepsy syndromes without structural brain abnormalities: clinical features and experimental modelsPharmacological enhancement of mGlu5 receptors rescues behavioral deficits in SHANK3 knock-out mice.Phenytoin inhibits the persistent sodium current in neocortical neurons by modifying its inactivation propertiesReduced sodium current in GABAergic interneurons in a mouse model of severe myoclonic epilepsy in infancyRole of the C-terminal domain in inactivation of brain and cardiac sodium channelsIdentification of an Nav1.1 sodium channel (SCN1A) loss-of-function mutation associated with familial simple febrile seizuresImpaired action potential initiation in GABAergic interneurons causes hyperexcitable networks in an epileptic mouse model carrying a human Na(V)1.1 mutationAction potential initiation in neocortical inhibitory interneurons.Phosphorylation of sodium channels mediated by protein kinase-C modulates inhibition by topiramate of tetrodotoxin-sensitive transient sodium currentNetwork topology of NaV1.7 mutations in sodium channel-related painful disorders.Unaltered Network Activity and Interneuronal Firing During Spontaneous Cortical Dynamics In Vivo in a Mouse Model of Severe Myoclonic Epilepsy of Infancy.Epileptogenic channelopathies: experimental models of human pathologies.Comparative neuronal differentiation of self-renewing neural progenitor cell lines obtained from human induced pluripotent stem cells.Nonfunctional NaV1.1 familial hemiplegic migraine mutant transformed into gain of function by partial rescue of folding defectsVoltage-gated sodium channels as therapeutic targets in epilepsy and other neurological disorders.Dravet syndrome: insights from in vitro experimental models.Na+ channelopathies and epilepsy: recent advances and new perspectives.Depletion of the Fragile X Mental Retardation Protein in Embryonic Stem Cells Alters the Kinetics of Neurogenesis.The X-Linked Intellectual Disability Protein IL1RAPL1 Regulates Dendrite Complexity.The impact of genetic and experimental studies on classification and therapy of the epilepsies.Rescuable folding defective NaV1.1 (SCN1A) mutants in epilepsy: properties, occurrence, and novel rescuing strategy with peptides targeted to the endoplasmic reticulum.Loss-of-function KCNH2 mutation in a family with long QT syndrome, epilepsy, and sudden death.Post-translational dysfunctions in channelopathies of the nervous system.Pure haploinsufficiency for Dravet syndrome Na(V)1.1 (SCN1A) sodium channel truncating mutations.A rescuable folding defective Nav1.1 (SCN1A) sodium channel mutant causes GEFS+: common mechanism in Nav1.1 related epilepsies?Self-limited hyperexcitability: functional effect of a familial hemiplegic migraine mutation of the Nav1.1 (SCN1A) Na+ channel.Beta-scorpion toxin effects suggest electrostatic interactions in domain II of voltage-dependent sodium channels.Molecular determinants for modulation of persistent sodium current by G-protein betagamma subunits.Action potentials recorded with patch-clamp amplifiers: are they genuine?A new type of scorpion Na+-channel-toxin-like polypeptide active on K+ channels.The 22nd ion channel meeting, september 2011, france.A BAC transgenic mouse model reveals neuron subtype-specific effects of a Generalized Epilepsy with Febrile Seizures Plus (GEFS+) mutation.Electroclinical features of a family with simple febrile seizures and temporal lobe epilepsy associated with SCN1A loss-of-function mutation.Functional and molecular defects of hiPSC-derived neurons from patients with ATM deficiencyProtein-kinase C-dependent phosphorylation inhibits the effect of the antiepileptic drug topiramate on the persistent fraction of sodium currents.First chemical synthesis of a scorpion alpha-toxin affecting sodium channels: the Aah I toxin of Androctonus australis hector.Layer-specific properties of the persistent sodium current in sensorimotor cortex.Pathophysiological mechanisms of migraine and epilepsy: Similarities and differences.Identification of two mutations in cis in the SCN1A gene in a family showing genetic epilepsy with febrile seizures plus (GEFS+) and idiopathic generalized epilepsy (IGE).Valproate selectively reduces the persistent fraction of Na+ current in neocortical neurons.
P50
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P50
description
hulumtues
@sq
onderzoeker
@nl
researcher
@en
հետազոտող
@hy
name
Massimo Mantegazza
@ast
Massimo Mantegazza
@en
Massimo Mantegazza
@es
Massimo Mantegazza
@nl
Massimo Mantegazza
@sl
type
label
Massimo Mantegazza
@ast
Massimo Mantegazza
@en
Massimo Mantegazza
@es
Massimo Mantegazza
@nl
Massimo Mantegazza
@sl
prefLabel
Massimo Mantegazza
@ast
Massimo Mantegazza
@en
Massimo Mantegazza
@es
Massimo Mantegazza
@nl
Massimo Mantegazza
@sl
P1053
J-8802-2016
P106
P21
P2798
P31
P3829
P496
0000-0002-1070-7929