N. Tabti

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Electromyography guides toward subgroups of mutations in muscle channelopathies

J. Willer, P. Laforêt, B. Eymard, 2004, Annals of neurology.

A study of synchronization of quantal transmitter release from mammalian motor endings by the use of botulinal toxins type A and D.

N. Tabti, J. Molgó, S. Thesleff, 1989, The Journal of physiology.

Presynaptic actions of botulinal neurotoxins at vertebrate neuromuscular junctions.

A. Mallart, J. Comella, N. Tabti, 1990, Journal de physiologie.

Lack of association of the potassium channel–associated peptide MiRP2-R83H variant with periodic paralysis

B. Hainque, B. Fontaine, E. Fournier, 2003, Neurology.

Hypokalemic periodic paralysis: A model for a clinical and research approach to a rare disorder

B. Fontaine, S. Vicart, E. Fournier, 2007, Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics.

Study on the induction of spontaneous transmitter release at early nerve-muscle contacts in Xenopus cultures

M. Poo, N. Tabti, 1994, Neuroscience Letters.

Physiological and ultrastructural features of human induced pluripotent and embryonic stem cell-derived skeletal myocytes in vitro

R. Perlingeiro, E. Fournier, N. Tabti, 2014, Proceedings of the National Academy of Sciences.

Pharmacological characterization of the calcium-insensitive, intermittent acetylcholine release at the rat neuromuscular junction.

N. Tabti, S. Thesleff, S. P. Yu, 1986, Acta physiologica Scandinavica.

Functional expression of the Ile693Thr Na+ channel mutation associated with paramyotonia congenita in a human cell line

A. George, B. Fontaine, N. Tabti, 1998, The Journal of physiology.

Hypokalaemic periodic paralysis type 2 caused by mutations at codon 672 in the muscle sodium channel gene SCN4A.

F. Lehmann-Horn, K. Jurkat-Rott, T. Maisonobe, 2001, Brain : a journal of neurology.

Clinical electrophysiology of muscle diseases and episodic muscle disorders.

Emmanuel Fournier, E. Fournier, N. Tabti, 2019, Handbook of Clinical Neurology.

Development of the excitation-contraction coupling machinery and its relation to myofibrillogenesis in human iPSC-derived skeletal myocytes

E. Fournier, N. Tabti, G. Skoglund, 2018, Skeletal Muscle.

Cold extends electromyography distinction between ion channel mutations causing myotonia

J. Willer, P. Laforêt, B. Eymard, 2006, Annals of neurology.

Screening identifies small molecules that enhance the maturation of human pluripotent stem cell-derived myotubes

R. Perlingeiro, W. Shen, A. Magli, 2019, eLife.

Terminal sprouting in mouse neuromuscular junctions poisoned with botulinum type a toxin: Morphological and electrophysiological features

J. Comella, N. Tabti, J. Molgó, 1990, Neuroscience.

Periodic paralysis and voltage-gated ion channels.

Bertrand Fontaine, B. Fontaine, N. Tabti, 1996, Kidney international.

Gating defects of a novel Na+ channel mutant causing hypokalemic periodic paralysis.

O. Devuyst, B. Fontaine, D. Sternberg, 2006, Biochemical and biophysical research communications.

A1152D mutation of the Na+ channel causes paramyotonia congenita and emphasizes the role of DIII/S4–S5 linker in fast inactivation

Magali Bouhours, J. Willer, B. Fontaine, 2005, The Journal of physiology.

Cold‐induced disruption of Na+ channel slow inactivation underlies paralysis in highly thermosensitive paramyotonia

B. Fontaine, E. Fournier, D. Sternberg, 2009, The Journal of physiology.

Mice transgenic for the human myotonic dystrophy region with expanded CTG repeats display muscular and brain abnormalities.

A. Delacourte, C. Junien, A. Ghestem, 2001, Human molecular genetics.

The nature and origin of calcium‐insensitive miniature end‐plate potentials at rodent neuromuscular junctions.

N. Tabti, S. Thesleff, F. Vyskocil, 1986, The Journal of physiology.

Three potassium currents in mouse motor nerve terminals

A. Mallart, N. Tabti, C. Bourret, 1989, Pflügers Archiv.

Pulsatile release of acetylcholine by nerve terminals (synaptosomes) isolated from Torpedo electric organ.

Y. Dunant, N. Tabti, M. Poo, 1992, The Journal of physiology.

Homozygosity for dominant mutations increases severity of muscle channelopathies

B. Eymard, B. Fontaine, C. Goizet, 2010, Muscle & nerve.

Functional characterization and cold sensitivity of T1313A, a new mutation of the skeletal muscle sodium channel causing paramyotonia congenita in humans

Magali Bouhours, J. Willer, B. Fontaine, 2004, The Journal of physiology.

Spontaneous synaptic activity at developing neuromuscular junctions.

M. Poo, N. Tabti, 1990, Progress in brain research.

Development of the excitation-contraction coupling machinery and its relation to myofibrillogenesis in human iPSC-derived skeletal myocytes

E. Fournier, N. Tabti, G. Skoglund, 2018, Skeletal Muscle.

Effects of some aminoquinolines on spontaneous quantal acetylcholine release.

N. Tabti, S. Thesleff, M. Lupa, 1986, Acta Physiologica Scandinavica.

[Detection of peripheral diabetic neuropathy. A reappraisal of electrophysiological data].

N. Tabti, F. Duron, M. Rieu, 1982, La Nouvelle presse medicale.

Unravelling the pathophysiology of calcium channel mutations causing neurological disorders.

B. Fontaine, N. Tabti, 2000, Brain : a journal of neurology.

Influence of muscle cells on the development of calcium currents in Xenopus spinal neurons

N. Tabti, L. Lhuillier, 1998, Neuroscience.