ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2006
Regulation of dendritic branching and spine maturation by semaphorin3A-Fyn signaling.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 93 papers.
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93 citing papers in PubMed, 172 citations in OpenAlex.
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- Contribution of the dihydropyrimidinase-like proteins family in synaptic physiology and in neurodevelopmental disorders.Frontiers in neuroscience · 2023Review
- SEMA6B variants cause intellectual disability and alter dendritic spine density and axon guidance.Human molecular genetics · 2022Article
- Enzymatic Degradation of Cortical Perineuronal Nets Reverses GABAergic Interneuron Maturation.Molecular neurobiology · 2022Article
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- Sex-specific accelerated decay in time/activity-dependent plasticity and associative memory in an animal model of Alzheimer's disease.Aging cell · 2021Article
- Activity-induced secretion of semaphorin 3A mediates learning.The European journal of neuroscience · 2021Article
- Semaphorin 3A contributes to sepsis‑induced immunosuppression by impairing CD4Molecular medicine reports · 2021Article
- Targeting Neuropilin-1 Suppresses the Stability of CD4Infection and immunity · 2021Article
- Post-status epilepticus treatment with the Fyn inhibitor, saracatinib, improves cognitive function in mice.BMC neuroscience · 2021Article
- Semaphorins in Adult Nervous System Plasticity and Disease.Frontiers in synaptic neuroscience · 2021Review
- NGF Signaling in Endosomes.Advances in experimental medicine and biology · 2021Article
33 more citing papers are in PubMed but not listed here.
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Authors and funding
12 authors at 5 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
A member of semaphorin family, semaphorin3A (Sema3A), acts as a chemorepellent or chemoattractant on a wide variety of axons and dendrites in the development of the nervous systems. We here show that Sema3A induces clustering of both postsynaptic density-95 (PSD-95) and presynaptic synapsin I in cultured cortical neurons without changing the density of spines or filopodia. Neuropilin-1 (NRP-1), a receptor for Sema3A, is present on both axons and dendrites. When the cultured neurons are exposed to Sema3A, the cluster size of PSD-95 is markedly enhanced, and an extensive colocalization of PSD-95 and NRP-1 or actin-rich protrusion is seen. The effects of Sema3A on spine morphology are blocked by PP2, an Src type tyrosine kinase inhibitor, but not by the PP3, the inactive-related compound. In the cultured cortical neurons from fyn(-/-) mice, dendrites bear few spines, and Sema3A does not induce PSD-95 cluster formation on the dendrites. Sema3A and its receptor genes are highly expressed during the synaptogenic period of postnatal days 10 and 15. The cortical neurons in layer V, but not layer III, show a lowered density of synaptic bouton-like structure on dendrites in sema3A- and fyn-deficient mice. The neurons of the double-heterozygous mice show the lowered spine density, whereas those of single heterozygous mice show similar levels of the spine density as the wild type. These findings suggest that the Sema3A signaling pathway plays an important role in the regulation of dendritic spine maturation in the cerebral cortex neurons.
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