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Molecular labeling, electrophysiology and calcium imaging have revealed a novel switching of neurotransmitter at the frog neuromuscular junction where motoneurons transiently release glutamate before acetylcholine at synapses on developing hindlimb muscles at the onset of metamorphosis.

A new tool enables electrophysiological isolation of input-specific neurotransmission in a powerful model glutamatergic circuit.

Synaptic partner recognition in the Drosophila neuromuscular circuit requires interactions between the Dpr and DIP subfamilies of immunoglobulin cell-surface proteins.

Depending upon the parameters used, neuromuscular stimulation can have beneficial or deleterious impacts on muscle structure and function in an animal model of Duchenne muscular dystrophy.

Ig domain family members DIP-alpha and Dpr10 are required in a subset of Drosophila leg motor neurons and muscles, respectively, to establish their fine terminal branching pattern and synapses.

Skeletal muscle cells constantly monitor their own activity and that of their partner neuron at synapses, enabling them to provide the neuron with feedback regarding neurotransmitter release.

Acting in neuronal stem cells, temporal transcription factors, as a class of molecules, are uniquely potent determinants of circuit membership that establish expected patterns of wiring in the motor system.

GDNF receptor-expressing mesenchymal progenitor subpopulation within skeletal muscle responds to peripheral nerve injury by sensing GDNF and secreting BDNF, thereby directly promoting nerve regeneration through facilitating remyelination by Schwann cells.

Maintenance of peripheral myonuclei patterning in skeletal myofibers is dependent on the regulation of microtubules dynamic and nuclei motion and is essential for proper neuromuscular junction integrity and mitochondria homeostasis.

An agonist antibody to MuSK, delivered after disease onset, decreases the loss of neuromuscular synapses, improves motor function and extends the lifespan of ALS mice.