Please use this identifier to cite or link to this item: https://doi.org/10.1523/JNEUROSCI.0163-13.2013
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dc.titleProBDNF and mature BDNF as punishment and reward signals for synapse elimination at mouse neuromuscular junctions
dc.contributor.authorShawn Je, H.
dc.contributor.authorYang, F.
dc.contributor.authorJi, Y.
dc.contributor.authorPotluri, S.
dc.contributor.authorFu, X.-Q.
dc.contributor.authorLuo, Z.-G.
dc.contributor.authorNagappan, G.
dc.contributor.authorChan, J.P.
dc.contributor.authorHempstead, B.
dc.contributor.authorSon, Y.-J.
dc.contributor.authorLu, B.
dc.date.accessioned2016-06-01T10:27:40Z
dc.date.available2016-06-01T10:27:40Z
dc.date.issued2013
dc.identifier.citationShawn Je, H., Yang, F., Ji, Y., Potluri, S., Fu, X.-Q., Luo, Z.-G., Nagappan, G., Chan, J.P., Hempstead, B., Son, Y.-J., Lu, B. (2013). ProBDNF and mature BDNF as punishment and reward signals for synapse elimination at mouse neuromuscular junctions. Journal of Neuroscience 33 (24) : 9957-9962. ScholarBank@NUS Repository. https://doi.org/10.1523/JNEUROSCI.0163-13.2013
dc.identifier.issn02706474
dc.identifier.urihttp://scholarbank.nus.edu.sg/handle/10635/124735
dc.description.abstractDuring development, mammalian neuromuscular junctions (NMJs) transit from multiple-innervation to single-innervation through axonal competition via unknown molecular mechanisms. Previously, using an in vitro model system, we demonstrated that the postsynaptic secretion of pro-brain-derived neurotrophic factor (proBDNF) stabilizes or eliminates presynaptic axon terminals, depending on its proteolytic conversion at synapses. Here, using developing mouse NMJs, we obtained in vivo evidence that proBDNF and mature BDNF (mBDNF) play roles in synapse elimination. We observed that exogenous proBDNF promoted synapse elimination, whereas mBDNF infusion substantially delayed synapse elimination. In addition, pharmacological inhibition of the proteolytic conversion of proBDNF to mBDNF accelerated synapse elimination via activation of p75 neurotrophin receptor (p75NTR). Furthermore, the inhibition of both p75NTR and sortilin signaling attenuated synapse elimination. We propose a model in which proBDNF and mBDNF serve as potential "punishment" and "reward" signals for inactive and active terminals, respectively, in vivo. © 2013 the authors.
dc.description.urihttp://libproxy1.nus.edu.sg/login?url=http://dx.doi.org/10.1523/JNEUROSCI.0163-13.2013
dc.sourceScopus
dc.typeArticle
dc.contributor.departmentDUKE-NUS GRADUATE MEDICAL SCHOOL S'PORE
dc.description.doi10.1523/JNEUROSCI.0163-13.2013
dc.description.sourcetitleJournal of Neuroscience
dc.description.volume33
dc.description.issue24
dc.description.page9957-9962
dc.description.codenJNRSD
dc.identifier.isiut000320235300011
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