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4-sulfation at the non-reducing end of chondroitin sulfate glycosaminoglycan chains is essential for inhibition of axonal growth.

Mature axons lose the ability to regenerate because key growth molecules are excluded through changes in vesicle transport, and restoring transport can restore regeneration.

Building on previous work (Liu et al., 2015), it is shown that depletion or rescue of adult skeletal muscle stem cells is sufficient to induce or attenuate age-associated neuromuscular junction deterioration respectively.

Single-cell RNA-sequencing unraveled cell subtype-specific transcriptomic changes in both injured and uninjured primary sensory neurons after nerve injury and demonstrated transcriptomic sexual dimorphism.

A murine model for a novel surgical concept demonstrates potential advances of neuroprosthetic interfacing.

Skeletal muscle stem cells play important roles in the regeneration of neuromuscular junctions, and so present new targets for therapies to treat neuromuscular decline observed in the context of aging and various neuromuscular diseases.

Close examination of lanceolate mechanosensory complexes has revealed clues about the ways that sensory nerves detect the movement of hairs and shown than terminal Schwann cells are needed to maintain and regenerate these intricate structures.

Whole mount 3D visualization of macromolecule synthesis with light sheet fluorescence microscopy enables quantitative, multiscale analysis at the organ, cellular, and molecular levels of organization.

Defects in synapse regeneration limit functional circuit recovery after nerve injury by misdirecting information via ectopic dendritic synapses, and also by functional and molecular deficits in reformed axonal synapses.

Despite lacking traditional ganglia or centralization, the Hydra nervous system computes sensorimotor responses via localized neuron ensembles.