Schwann Cells Promote Synaptogenesis at the Neuromuscular Junction via Transforming Growth Factor-β1

Feng, Zhichun; Ko, Chien‐Ping

doi:10.1523/jneurosci.2589-08.2008

Cited by 129 publications

(117 citation statements)

References 58 publications

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“…In particular, TGF-β1 was identified as the molecule responsible for the synaptogenesis promiting effect of Schwann cell-conditioned medium in Xenopus nerve-muscle cocultures (Feng & Ko, 2008). TGF-β1 increased agrin expression and synaptogenesis were along nerve-muscle contacts while immunodepletion of TGF-β1 with a specific antibody abolished the synaptogenic effect of Schwann cell-conditioned medium (Feng & Ko, 2008). These results indicate that TGF-β1 may be a glial signal that instructs neurons to switch from a "growth state" to a "synaptogenic state".…”

Section: Synaptic Transmission and Plasticitymentioning

confidence: 99%

Transforming Growth Factor Beta in the Central Nervous System

Dobolyi¹

2012

Neuroscience - Dealing With Frontiers

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Section: Synaptic Transmission and Plasticitymentioning

confidence: 99%

Transforming Growth Factor Beta in the Central Nervous System

Dobolyi¹

2012

Neuroscience - Dealing With Frontiers

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“…Several factors have been implicated in motoneuron survival or synapse elimination including glial cell line-derived neurotrophic factor (GDNF) and brain-derived neurotrophic factor (BDNF) (Oppenheim et al, 1995;Nguyen et al, 1998;Keller-Peck et al, 2001;Lu and Je, 2003). Transforming growth factor  (TGF), fibroblast growth factor (FGF), laminin and collagen appear to play a role in orchestrating presynaptic development at the NMJ (McCabe et al, 2003;Rawson et al, 2003;Nishimune et al, 2004;Fox et al, 2007;Feng and Ko, 2008;Nishimune et al, 2008). Previously, we demonstrated that phrenic nerve branches are mislocated and synaptic vesicle release is compromised in mice lacking -catenin in muscles , suggesting a necessary role of muscle -catenin for presynaptic differentiation or function.…”

Section: Introductionmentioning

confidence: 99%

β-Catenin gain of function in muscles impairs neuromuscular junction formation

Barik

et al. 2012

Development

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“…For example, Schwann cells might guide motoneuron growth cones (Reddy et al, 2003), as they sprout and guide nerve terminal regeneration after nerve injury (Reynolds and Woolf, 1992;Son and Thompson, 1995a;Son and Thompson, 1995b). They have also been shown to generate diffusible signals, one of which might be transforming growth factor b (TGFb) (Feng and Ko, 2008), to promote NMJ development or function (Cao and Ko, 2007). This is similar to astrocytes, which regulate CNS synaptogenesis through diffusible factors (Christopherson et al, 2005).…”

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confidence: 99%

“…Their neonatal death is probably due to the aberrant transmission of signals from the respiratory center in the brain. A recent study suggests that TGFb1 might act as a Schwann cell-derived factor to promote NMJ formation in Xenopus, probably by increasing agrin expression in motoneurons (Feng and Ko, 2008), highlighting the complexity of the cellular and molecular interactions in this relatively simple structure. …”

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confidence: 99%

To build a synapse: signaling pathways in neuromuscular junction assembly

2010

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SummarySynapses, as fundamental units of the neural circuitry, enable complex behaviors. The neuromuscular junction (NMJ) is a synapse type that forms between motoneurons and skeletal muscle fibers and that exhibits a high degree of subcellular specialization. Aided by genetic techniques and suitable animal models, studies in the past decade have brought significant progress in identifying NMJ components and assembly mechanisms. This review highlights recent advances in the study of NMJ development, focusing on signaling pathways that are activated by diffusible cues, which shed light on synaptogenesis in the brain and contribute to a better understanding of muscular dystrophy. Key words: Neural development, Neuromuscular junction, Retrograde signaling, Synapse formation IntroductionThe brain contains billions of nerve cells, or neurons, which receive and integrate signals from the environment, and which govern the body's responses. Nervous system activity is made possible by synapses, contacts formed either between neurons or between a neuron and a target cell. Synapses are asymmetric structures in which neurotransmitter molecules are released from the presynaptic membrane and activate receptors on the postsynaptic membrane, thus establishing neuronal communication. As such, synapses are fundamental units of neural circuitry and enable complex behaviors. The neuromuscular junction (NMJ) is a type of synapse formed between motoneurons and skeletal muscle fibers. Large and easily accessed experimentally, this peripheral synapse has contributed greatly to the understanding of the general principles of synaptogenesis and to the development of potential therapeutic strategies for muscular disorders. The NMJ uses different neurotransmitters in different species; for example, acetylcholine (ACh) in vertebrates and glutamate in Drosophila, both of which are excitatory and cause muscle contraction. In Caenorhabditis elegans, there are two types of NMJs: at excitatory NMJs, ACh causes muscle contraction, whereas inhibitory NMJs release g-aminobutyric acid (GABA) to cause muscle relaxation. Motor nerve terminals differentiate to form presynaptic active zones, where synaptic vesicles dock and release neurotransmitters. On the apposed postsynaptic membranes, neurotransmitter receptors are packed at high densities. Aided by genetic techniques and by the use of suitable animal models, including rodents, zebrafish, Drosophila and C. elegans, studies in the past decade have brought significant progress, not only in identifying components present in pre-and postsynaptic membranes, but also in understanding the mechanisms that underpin NMJ assembly. This review highlights recent advances in the study of NMJ development, focusing on signaling pathways that are activated by diffusible cues from motor nerves and muscle fibers. Readers are referred to other outstanding reviews for a broad view of NMJ development (see Froehner, 1993;Hall and Sanes, 1993;Kummer et al., 2006;Salpeter and Loring, 1985;Schaeffer et al., 2001). NMJ formati...

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Schwann Cells Promote Synaptogenesis at the Neuromuscular Junction via Transforming Growth Factor-β1

Cited by 129 publications

References 58 publications

Transforming Growth Factor Beta in the Central Nervous System

Transforming Growth Factor Beta in the Central Nervous System

β-Catenin gain of function in muscles impairs neuromuscular junction formation

To build a synapse: signaling pathways in neuromuscular junction assembly

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