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Article: Differential effects of neurotrophins and schwann cell-derived signals on neuronal survival/growth and synaptogenesis

TitleDifferential effects of neurotrophins and schwann cell-derived signals on neuronal survival/growth and synaptogenesis
Authors
KeywordsNeurotrophins
Neuromuscular junction
NMJ
Agrin
Schwann cell
Synaptogenesis
Neuronal survival
Issue Date2003
PublisherSociety for Neuroscience. The Journal's web site is located at http://www.jneurosci.org
Citation
The Journal of Neuroscience, 2003, v. 23 n. 12, p. 5050-5060 How to Cite?
AbstractRecent 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.
Persistent Identifierhttp://hdl.handle.net/10722/225411
ISSN
2015 Impact Factor: 5.924
2015 SCImago Journal Rankings: 5.105

 

DC FieldValueLanguage
dc.contributor.authorPeng, HB-
dc.contributor.authorYang, JF-
dc.contributor.authorDai, Z-
dc.contributor.authorLee, CW-
dc.contributor.authorHung, HW-
dc.contributor.authorFeng, ZH-
dc.contributor.authorKo, CP-
dc.date.accessioned2016-05-06T02:03:49Z-
dc.date.available2016-05-06T02:03:49Z-
dc.date.issued2003-
dc.identifier.citationThe Journal of Neuroscience, 2003, v. 23 n. 12, p. 5050-5060-
dc.identifier.issn0270-6474-
dc.identifier.urihttp://hdl.handle.net/10722/225411-
dc.description.abstractRecent 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.-
dc.languageeng-
dc.publisherSociety for Neuroscience. The Journal's web site is located at http://www.jneurosci.org-
dc.relation.ispartofThe Journal of Neuroscience-
dc.rightsThe Journal of Neuroscience. Copyright © Society for Neuroscience.-
dc.subjectNeurotrophins-
dc.subjectNeuromuscular junction-
dc.subjectNMJ-
dc.subjectAgrin-
dc.subjectSchwann cell-
dc.subjectSynaptogenesis-
dc.subjectNeuronal survival-
dc.titleDifferential effects of neurotrophins and schwann cell-derived signals on neuronal survival/growth and synaptogenesis-
dc.typeArticle-
dc.identifier.emailLee, CW: chiwai.lee@hku.hk-
dc.identifier.authorityLee, CW=rp02089-
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.pmid12832528-
dc.identifier.volume23-
dc.identifier.issue12-
dc.identifier.spage5050-
dc.identifier.epage5060-
dc.publisher.placeUnited States-

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