ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2022
The Nogo-66 Receptors NgR1 and NgR3 Are Required for Commissural Axon Pathfinding.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 18 citations in OpenAlex.
- Molecular continuity between axon guidance and synaptic function.Molecules and cells · 2026Review
- The therapeutic potential and mechanisms of targeting the PTBP1/Nogo-A/NgR axis in PTSD induced by single prolonged stress in mice.Experimental & molecular medicine · 2026Article
- Probing the role of synaptic adhesion molecule RTN4RL2 in setting up cochlear connectivity.eLife · 2025Article
- Animal Models of Human Disease 2.0.International journal of molecular sciences · 2024Article
- Article
- Differential expression of genes in the RhoA/ROCK pathway in the hippocampus and cortex following intermittent hypoxia and high-intensity interval training.Journal of neurophysiology · 2024Article
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Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Nogo-66 receptors (NgR1-3) are glycosylphosphatidyl inositol-linked proteins that belong to the leucine-rich repeat superfamily. Through binding to myelin-associated inhibitors, NgRs contribute to the inhibition of axonal regeneration after spinal cord injury. Their role in limiting synaptic plasticity and axonal outgrowth in the adult CNS has been described previously, but not much is known about their role during the development of the nervous system. Here, we show that NgR1 and NgR3 mRNAs are expressed during spinal cord development of the chicken embryo. In particular, they are expressed in the dI1 subpopulation of commissural neurons during the time when their axons navigate toward and across the floorplate, the ventral midline of the spinal cord. To assess a potential role of NgR1 and NgR3 in axon guidance, we downregulated them using
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