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

Content Provider	PubMed Central
Author	Feng, Zhihua Ko, Chien-ping
Copyright Year	2008
Abstract	Recent studies suggest that glial cells actively participate in the formation, function, maintenance, and repair of the chemical synapse. However, the molecular mechanisms of glia–synapse interactions are largely unknown. We have shown previously that Schwann cell-conditioned medium (SC-CM) promotes synaptogenesis in Xenopus nerve–muscle cocultures. The present study aimed to identify the synaptogenic molecules in SC-CM. Combining biochemical approaches and in vitro bioassays, we found that SC-CM contains transforming growth factor (TGF)-β1, which is expressed in Schwann cells both in vivo and in vitro. Similar to SC-CM, TGF-β1 doubled the size of acetylcholine receptor (AChR) clusters at nerve–muscle contacts and significantly increased the percentage of nerve–muscle contacts that show AChR clusters to ∼60%, compared with ∼20% seen in control cultures. The synaptogenic effects of SC-CM were abolished if SC-CM was immunodepleted of TGF-β1 or if the latency-associated protein or a TGF-β1 receptor kinase inhibitor was added to block the bioactivity of TGF-β1. Similar to frog SC-CM, mammalian SC-CM also showed synaptogenic effects, which were prevented by immunodepletion of TGF-β1. TGF-β1 upregulated agrin expression in spinal neurons, which could explain the increase in AChR clusters in cultures treated with SC-CM. These results suggest that Schwann cells express TGF-β1, which is both sufficient and necessary for mediating the synapse-promoting effects of Schwann cells at the developing neuromuscular junction. Schwann cell-derived TGF-β1 thus joins other astrocyte-derived synaptogenic factors in further strengthening the emerging concept that glial cells contribute to synaptogenesis in both the PNS and the CNS.
Related Links	http://dx.doi.org/10.1523/jneurosci.2589-08.2008
Ending Page	9609
Page Count	11
Starting Page	9599
File Format	PDF
ISSN	02706474
e-ISSN	15292401
Journal	The Journal of Neuroscience
Issue Number	39
Volume Number	28
Language	English
Publisher	Society for Neuroscience
Publisher Date	2008-09-24
Access Restriction	Open
Rights Holder	Society for Neuroscience
Subject Keyword	Neuroscience(all) Research in Higher Education
Content Type	Text
Resource Type	Article
Subject	Neuroscience

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