Thomas W. Gould1, Chien-Ping Ko2, Hugh Willison3 and Richard Robitaille4,5 1Department of Physiology and Cell Biology, University of Nevada, Reno School of Medicine, Reno, Nevada 89557, USA 2Section of Neurobiology, Department of Biological Sciences, University of Southern California, Los Angeles, California 90089-2520, USA 3School of Infection and Immunity, University of Glasgow, Glasgow G12 8TA, Scotland 4Département de neurosciences, Université de Montréal, Montréal, Québec H3C 3J7, Canada 5Centre Interdisciplinaire de Recherche sur le Cerveau et l'apprentissage, Université de Montréal, Montréal, Québec H3C 3J7, Canada Correspondence: richard.robitailleumontreal.ca

The neuromuscular junction (NMJ) is a highly reliable synapse to carry the control of the motor commands of the nervous system over the muscles. Its development, organization, and synaptic properties are highly structured and regulated to support such reliability and efficacy. Yet, the NMJ is also highly plastic, able to react to injury, and able to adapt to changes. This balance between structural stability and synaptic efficacy on one hand and structural plasticity and repair on another hand is made possible by perisynaptic Schwann cells (PSCs), glial cells at this synapse. They regulate synaptic efficacy and structural plasticity of the NMJ in a dynamic, bidirectional manner owing to their ability to decode synaptic transmission and by their interactions with trophic-related factors. Alteration of these fundamental roles of PSCs is also important in the maladapted response of NMJs in various diseases and in aging.