ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2003
Differential effects of neurotrophins and schwann cell-derived signals on neuronal survival/growth and synaptogenesis.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.
What it found
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Who cites it
48 citing papers in PubMed, 126 citations in OpenAlex.
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- Mind In Vitro Platforms: Versatile, Scalable, Robust, and Open Solutions to Interfacing with Living Neurons.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- Response of terminal Schwann cells following volumetric muscle loss injury.Experimental neurology · 2023Article
- Nerve-independent formation of membrane infoldings at topologically complex postsynaptic apparatus by caveolin-3.Science advances · 2023Article
- Peripheral glia diversity.Journal of anatomy · 2022Review
- Principles for the design of multicellular engineered living systems.APL bioengineering · 2022Article
- hiPSC-Derived Schwann Cells Influence Myogenic Differentiation in Neuromuscular Cocultures.Cells · 2021Article
- Ketamine Alters Functional Plasticity of Astroglia: An Implication for Antidepressant Effect.Life (Basel, Switzerland) · 2021Review
- Cross-talk between motor neurons and myotubes via endogenously secreted neural and muscular growth factors.Physiological reports · 2021Article
- Ketamine Action on Astrocytes Provides New Insights into Rapid Antidepressant Mechanisms.Advances in neurobiology · 2021Review
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- Overview of Impaired BDNF Signaling, Their Coupled Downstream Serine-Threonine Kinases and SNARE/SM Complex in the Neuromuscular Junction of the Amyotrophic Lateral Sclerosis Model SOD1-G93A Mice.Molecular neurobiology · 2019Article
- Optogenetic stimulation promotes Schwann cell proliferation, differentiation, and myelination in vitro.Scientific reports · 2019Article
- In Vitro Innervation as an Experimental Model to Study the Expression and Functions of Acetylcholinesterase and Agrin in Human Skeletal Muscle.Molecules (Basel, Switzerland) · 2017Review
- Presynaptic Membrane Receptors Modulate ACh Release, Axonal Competition and Synapse Elimination during Neuromuscular Junction Development.Frontiers in molecular neuroscience · 2017Review
- Schwann Cells in Neuromuscular Junction Formation and Maintenance.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2016Article
- A system for studying mechanisms of neuromuscular junction development and maintenance.Development (Cambridge, England) · 2016Article
Corrections and comments
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Authors and funding
7 authors at 1 institution in 2 countries.
Funding
Abstract
Recent studies have shown that the survival of mammalian motoneurons in vitro is promoted by neurotrophins (NTs) and cAMP. There is also evidence that neurotrophins enhance transmitter release. We thus investigated whether these agents also promote synaptogenesis. Cultured Xenopus spinal cord neurons were treated with a mixture of BDNF, glia-derived neurotrophic factor, NT-3, and NT-4, in addition to forskolin and IBMX or the cell-permeant form of cAMP, to elevate the cAMP level. The outgrowth and survival of neurons were dramatically increased by this trophic stimulation. However, when these neurons were cocultured with muscle cells, the trophic agents resulted in a failure of synaptogenesis. Specifically, the induction of ACh receptor (AChR) clustering in cultured muscle cells was inhibited at nerve-muscle contacts, in sharp contrast to control, untreated cocultures. Because AChR clustering induced by agrin or growth factor-coated beads in muscle cells was unaffected by trophic stimulation, its effect on synaptogenesis is presynaptic in origin. In the control, agrin was deposited along the neurite and at nerve-muscle contacts. This was significantly downregulated in cultures treated with trophic stimuli. Reverse transcriptase-PCR analyses showed that this decrease in agrin deposition was caused by an inhibition of agrin synthesis by trophic stimuli. Both agrin synthesis and induction of AChR clustering were restored under trophic stimulation when Schwann cell-conditioned medium was introduced. These results suggest that trophic stimulation maintains spinal neurons in the growth state, and Schwann cell-derived factors allow them to switch to the synaptogenic state.
Indexed as
Identifiers
12832528PMC6741189W2137999108What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.