ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2010
Combined genetic attenuation of myelin and semaphorin-mediated growth inhibition is insufficient to promote serotonergic axon regeneration.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers.
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Who cites it
50 citing papers in PubMed, 78 citations in OpenAlex.
- Article
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- Lactate promotes microglial scar formation and facilitates locomotor function recovery by enhancing histone H4 lysine 12 lactylation after spinal cord injury.Journal of neuroinflammation · 2024Article
- Regulation of axonal regeneration after mammalian spinal cord injury.Nature reviews. Molecular cell biology · 2023Review
- Chronic spinal cord injury repair by NT3-chitosan only occurs after clearance of the lesion scar.Signal transduction and targeted therapy · 2022Article
- Capacity of astrocytes to promote axon growth in the injured mammalian central nervous system.Frontiers in neuroscience · 2022Review
- LZK-dependent stimulation of astrocyte reactivity promotes corticospinal axon sprouting.Frontiers in cellular neuroscience · 2022Article
- Neuronal Redevelopment and the Regeneration of Neuromodulatory Axons in the Adult Mammalian Central Nervous System.Frontiers in cellular neuroscience · 2022Review
- Modulation of Both Intrinsic and Extrinsic Factors Additively Promotes Rewiring of Corticospinal Circuits after Spinal Cord Injury.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2021Article
- Unraveling Axon Guidance during Axotomy and Regeneration.International journal of molecular sciences · 2021Review
- Vinaxanthone inhibits Semaphorin3A induced axonal growth cone collapse in embryonic neurons but fails to block its growth promoting effects on adult neurons.Scientific reports · 2021Article
- EFA6 in Axon Regeneration, as a Microtubule Regulator and as a Guanine Nucleotide Exchange Factor.Cells · 2021Review
- Targeting axon guidance cues for neural circuit repair after spinal cord injury.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2021Article
- Olig2-Induced Semaphorin Expression Drives Corticospinal Axon Retraction After Spinal Cord Injury.Cerebral cortex (New York, N.Y. : 1991) · 2020Article
- Restoring Cellular Energetics Promotes Axonal Regeneration and Functional Recovery after Spinal Cord Injury.Cell metabolism · 2020Article
- Catecholaminergic axons in the neocortex of adult mice regrow following brain injury.Experimental neurology · 2020Article
- Integrins promote axonal regeneration after injury of the nervous system.Biological reviews of the Cambridge Philosophical Society · 2018Review
- Dissecting spinal cord regeneration.Nature · 2018Review
- Serotonin axons in the neocortex of the adult female mouse regrow after traumatic brain injury.Journal of neuroscience research · 2018Article
- Review
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
After CNS injuries, axon growth inhibitors from the myelin and the scar tissue at the injury site are considered major impediments to axon regeneration. The presence of several classes of inhibitors with multiple members in each class suggests functional redundancy in growth inhibition. To test redundancy within the myelin inhibitory pathway, we analyzed raphe spinal serotonergic (5-HT) axon regeneration in mice deficient in two major myelin inhibitors, Nogo and MAG, and their common receptor NgR1 (or NgR). After a complete transection spinal cord injury, there was no significant enhancement of 5-HT axon regeneration beyond the injury site in either Nogo/MAG/NgR1 triple mutants or NgR1 single mutants. Occasional, genotype-independent traversal of 5-HT axons through GFAP-positive tissue bridges at the injury site implicates GFAP-negative lesion areas as especially inhibitory to 5-HT axons. To assess the contribution of class 3 Semaphorins that are expressed by GFAP-negative meningeal fibroblasts at the injury site, we analyzed mice deficient in PlexinA3 and PlexinA4, two key receptors for class 3 Semaphorins, with or without additional NgR1 deletion. No enhanced regeneration of 5-HT or corticospinal axons was detected in PlexinA3/PlexinA4 double mutants or PlexinA3/PlexinA4/NgR1 triple mutants through a complete transection injury. In contrast with previous reports, these data demonstrate that attenuating myelin or Semaphorin-mediated inhibition of axon growth is insufficient to promote 5-HT axon regeneration and further indicate that even attenuating both classes of inhibitory influences is insufficient to promote regeneration of injured axons through a complete transection spinal cord injury.
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