N. Tabti

A review on drugs and toxins affecting presynaptic K+ currents and phasic quantal transmitter release at motor nerve terminals.

1989Acta physiologica et pharmacologica latinoamericana : organo de la Asociacion Latinoamericana de Ciencias Fisiologicas y de la Asociacion Latinoamericana de Farmacologia4 citations

Semantic Scholar

N. Tabti

Most-cited papers

Electromyography guides toward subgroups of mutations in muscle channelopathies

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

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

Cold extends electromyography distinction between ion channel mutations causing myotonia

Terminal sprouting in mouse neuromuscular junctions poisoned with botulinum type A toxin: morphological and electrophysiological features.

Presynaptic actions of botulinal neurotoxins at vertebrate neuromuscular junctions.

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

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

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

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

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

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

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

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

Homozygosity for dominant mutations increases severity of muscle channelopathies

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

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

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

Three potassium currents in mouse motor nerve terminals

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

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

Clinical electrophysiology of muscle diseases and episodic muscle disorders.

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

Effects of some aminoquinolines on spontaneous quantal acetylcholine release.

A review on drugs and toxins affecting presynaptic K+ currents and phasic quantal transmitter release at motor nerve terminals.

Facilitation, augmentation and potentiation of transmitter release at frog neuromuscular junctions poisoned with botulinum toxin

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

Electrophysiological studies of the sciatic nerves in Mycobacterium leprae foot pad-injected rats.

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

Generation of a mouse model for Schwartz–Jampel syndrome