Associated Papers
The astrocytic engine: Na+,K+-ATPase at the nexus of brain function and malfunction.
Verkhratsky A et al.
American Journal of Physiology. Cell Physiology, 2026
Spontaneous spreading depolarizations originate subcortically in a novel mouse model of familial hemiplegic migraine type 2.
Jansen NA et al.
Neurobiology of Disease, 2024
Astrocytic Na+, K+ ATPases in physiology and pathophysiology.
Pietrobon D et al.
Cell Calcium, 2024
Pathophysiology of migraine aura.
Sanchez Del Rio M et al.
Handbook of Clinical Neurology, 2023
Genetics of migraine: Delineation of contemporary understanding of the genetic underpinning of migraine.
de Boer I et al.
Handbook of Clinical Neurology, 2023
Hyperexcitable interneurons trigger cortical spreading depression in an Scn1a migraine model.
Auffenberg E et al.
The Journal of Clinical Investigation, 2021
Functional correlation of ATP1A2 mutations with phenotypic spectrum: from pure hemiplegic migraine to its variant forms.
Li Y et al.
The Journal of Headache and Pain, 2021
Non-canonical glutamate signaling in a genetic model of migraine with aura.
Parker PD et al.
Neuron, 2021
Astrocyte deletion of α2-Na/K ATPase triggers episodic motor paralysis in mice via a metabolic pathway.
Smith SE et al.
Nature Communications, 2020
Characteristics of cortical spreading depression and c-Fos expression in transgenic mice having a mutation associated with familial hemiplegic migraine 2.
Tang C et al.
Cephalalgia : an International Journal of Headache, 2020
Genetics of migraine aura: an update.
de Boer I et al.
The Journal of Headache and Pain, 2020
Cell biology and dynamics of Neuronal Na+/K+-ATPase in health and diseases.
Shrivastava AN et al.
Neuropharmacology, 2020
Astrocyte dysfunction increases cortical dendritic excitability and promotes cranial pain in familial migraine.
Romanos J et al.
Science Advances, 2020
Na+/K+-ATPase α isoform deficiency results in distinct spreading depolarization phenotypes.
Reiffurth C et al.
Journal of Cerebral Blood Flow and Metabolism : Official Journal of the International Society of Cerebral Blood Flow and Metabolism, 2020
A Chinese family with familial hemiplegic migraine type 2 due to a novel missense mutation in ATP1A2.
Tang W et al.
Cephalalgia : an International Journal of Headache, 2019
Differential effect of FHM2 mutation on synaptic plasticity in distinct hippocampal regions.
Iure A et al.
Cephalalgia : an International Journal of Headache, 2019
Genetic mouse models of migraine.
Pietrobon D et al.
The Journal of Headache and Pain, 2019
Mouse Models of Familial Hemiplegic Migraine for Studying Migraine Pathophysiology.
Dehghani A et al.
Current Neuropharmacology, 2019
Increased susceptibility to cortical spreading depression and epileptiform activity in a mouse model for FHM2.
Kros L et al.
Scientific Reports, 2018
The α2β2 isoform combination dominates the astrocytic Na+ /K+ -ATPase activity and is rendered nonfunctional by the α2.G301R familial hemiplegic migraine type 2-associated mutation.
Stoica A et al.
Glia, 2017
Recurrent coma and fever in familial hemiplegic migraine type 2. A prospective 15-year follow-up of a large family with a novel ATP1A2 mutation.
Pelzer N et al.
Cephalalgia : an International Journal of Headache, 2017
Genetics of Migraine: Insights into the Molecular Basis of Migraine Disorders.
Sutherland HG et al.
Headache, 2017
Genetic insights into migraine and glutamate: a protagonist driving the headache.
Gasparini CF et al.
Journal of the Neurological Sciences, 2016
Defective glutamate and K+ clearance by cortical astrocytes in familial hemiplegic migraine type 2.
Capuani C et al.
Embo Molecular Medicine, 2016
Animal models of monogenic migraine.
Chen SP et al.
Cephalalgia : an International Journal of Headache, 2016
Glutamate-system defects behind psychiatric manifestations in a familial hemiplegic migraine type 2 disease-mutation mouse model.
Bøttger P et al.
Scientific Reports, 2016
Insights into the Pathology of the α2-Na(+)/K(+)-ATPase in Neurological Disorders; Lessons from Animal Models.
Isaksen TJ et al.
Frontiers in Physiology, 2016
ATP1A2 Mutations in Migraine: Seeing through the Facets of an Ion Pump onto the Neurobiology of Disease.
Friedrich T et al.
Frontiers in Physiology, 2016
Migraine pathophysiology: lessons from mouse models and human genetics.
Ferrari MD et al.
The Lancet. Neurology, 2015
[Genetics of primary headache syndromes].
Freilinger T
Bundesgesundheitsblatt, Gesundheitsforschung, Gesundheitsschutz, 2014
Functional analysis of human Na(+)/K(+)-ATPase familial or sporadic hemiplegic migraine mutations expressed in Xenopus oocytes.
Spiller S et al.
World Journal of Biological Chemistry, 2014
Calcium channels and synaptic transmission in familial hemiplegic migraine type 1 animal models.
Uchitel OD et al.
Biophysical Reviews, 2014
A novel ATP1A2 gene mutation in familial hemiplegic migraine and epilepsy.
Costa C et al.
Cephalalgia : an International Journal of Headache, 2014
Familial hemiplegic migraine mutations affect Na,K-ATPase domain interactions.
Swarts HG et al.
Biochimica Et Biophysica Acta, 2013
Pearls and pitfalls in genetic studies of migraine.
Eising E et al.
Cephalalgia : an International Journal of Headache, 2013
Genetic effects of ATP1A2 in familial hemiplegic migraine type II and animal models.
Gritz SM et al.
Human Genomics, 2013
Migraine: a disorder of brain excitatory-inhibitory balance?
Vecchia D et al.
Trends in Neurosciences, 2012
Neurovascular changes in prolonged migraine aura in FHM with a novel ATP1A2 gene mutation.
Iizuka T et al.
Journal of Neurology, Neurosurgery, and Psychiatry, 2012
Migraine- and dystonia-related disease-mutations of Na+/K+-ATPases: relevance of behavioral studies in mice to disease symptoms and neurological manifestations in humans.
Bøttger P et al.
Neuroscience and Biobehavioral Reviews, 2012
CaV2.1 voltage activated calcium channels and synaptic transmission in familial hemiplegic migraine pathogenesis.
Uchitel OD et al.
Journal of Physiology, Paris, 2012
Increased susceptibility to cortical spreading depression in the mouse model of familial hemiplegic migraine type 2.
Leo L et al.
Plos Genetics, 2011
The structure of the Na+,K+-ATPase and mapping of isoform differences and disease-related mutations.
Morth JP et al.
Philosophical Transactions of the Royal Society of London. Series B, Biological Sciences, 2009
Diverse functional consequences of mutations in the Na+/K+-ATPase alpha2-subunit causing familial hemiplegic migraine type 2.
Tavraz NN et al.
The Journal of Biological Chemistry, 2008
Epilepsy as part of the phenotype associated with ATP1A2 mutations.
Deprez L et al.
Epilepsia, 2008