Validated mathematical relationships between motoneuron morphometric and electrophysiological properties are provided as a tool for neuroscientists and modellers to generate hypotheses for experimental studies investigating currently unreported relationships and build virtual motoneuron profiles with consistent properties for modelling purposes.

Motoneuron activity provides feedback to the spinal network responsible for generating locomotion in the developing mouse spinal cord.

Electrophysiological analyses reveal interactions between gasotransmitter enzymes and their respective products that regulate hypoglossal motoneuron excitability and may drive changes in upper airway tone in obstructive sleep apnea and perturb behaviors such as vocalization and swallowing.

Contrary to a long-standing hypothesis, the neuronal death that leads to muscle wastage in amyotrophic lateral sclerosis does not result from overactivity of those neurons during development.

The pain mediator bradykinin was found to sensitize spinal motoneurons by a direct postsynaptic action, questioning the role of motoneurons in the assessment of hyperalgesia since the withdrawal motor reflex is commonly used as a surrogate pain model.

Electrophysiological recordings from mouse spinal motoneurons reveal key roles for ion channels in establishing the differential activation of motoneuron subtypes during postnatal development.

A novel role of motoneuron Wnts in regulating presynaptic development at the neuromuscular junction.

Major differences among the main spinal V1 inhibitory interneuron subgroups were revealed based on neurogenesis, circuit placement, and motoneuron targeting, and Foxp2-V1 interneurons were identified tightly coupled to limb control.

The amount of secreted Pgk1 is sharply decreased in Rtn4al/NogoA-overexpressed muscle cells, leading to various manifestations of neurodegenerative disease, including denervated neuromuscular junction and failed neurite outgrowth of motoneurons.

Analysis of embryonic mouse diaphragm reveals muscle and nerve left–right asymmetries set by a Nodal-dependent genetic cascade, which imprints different molecular signatures to left and right motoneurons that shape their innervation pattern.