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  N-cadherin transsynaptically regulates short-term plasticity at glutamatergic synapses in embryonic stem cell-derived neurons

Jüngling, K., Eulenburg, V., Moore, R., Kemler, R., Lessmann, V., & Gottmann, K. (2006). N-cadherin transsynaptically regulates short-term plasticity at glutamatergic synapses in embryonic stem cell-derived neurons. Journal of Neuroscience, 26(26), 6968-6978. doi:10.1523/JNEUROSCI.1013-06.2006.

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Jüngling, Kay, Author
Eulenburg, Volker, Author
Moore, Robert, Author
Kemler, Rolf, Author
Lessmann, Volkmar, Author
Gottmann, Kurt1, Author           
Affiliations:
1Molecular neurobiology, Max Planck Institute of Experimental Medicine, Max Planck Society, ou_2173659              

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Free keywords: synaptic adhesion molecules; cadherins; synaptic depression; facilitation; retrograde regulation; ES cell-derived neurons SYNAPTIC VESICLE CYCLE; ADHESION MOLECULES; BETA-CATENIN; EXCITATORY SYNAPSES; HIPPOCAMPAL-NEURONS; RELEASE; ACTIN; CONNECTIONS; SYSTEM; CNS
 Abstract: The cell adhesion molecule N-cadherin has been proposed to regulate synapse formation in mammalian central neurons. This is based on its synaptic localization enabling alignment of presynaptic and postsynaptic specializations by an adhesion mechanism. However, a potential role of N-cadherin in regulating synaptic transmission has remained elusive. In this paper, a functional analysis of N-cadherin knock-out synapses was enabled by in vitro neuronal differentiation of mouse embryonic stem cells circumventing the early embryonic lethality of mice genetically null for N-cadherin. In our in vitro system, initial synapse formation was not altered in the absence of N-cadherin, which might be attributable to compensatory mechanisms. Here, we demonstrate that N-cadherin is required for regulating presynaptic function at glutamatergic synapses. An impairment in the availability of vesicles for exocytosis became apparent selectively during high activity. Short-term plasticity was strongly altered with synaptic depression enhanced in the absence of N-cadherin. Most intriguingly, facilitation was converted to depression under specific stimulation conditions. This indicates an important role of N-cadherin in the control of short-term plasticity. To analyze, whether N-cadherin regulates presynaptic function by a transsynaptic mechanism, we studied chimeric cultures consisting of wild-type neocortical neurons and ES cell-derived neurons. With N-cadherin absent only postsynaptically, we observed a similar increase in short-term synaptic depression as found in its complete absence. This indicates a retrograde control of short-term plasticity by N-cadherin. In summary, our results revealed an unexpected involvement of a synaptic adhesion molecule in the regulation of short-term plasticity at glutamatergic synapses.

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Language(s): eng - English
 Dates: 2006-06
 Publication Status: Published in print
 Pages: -
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 Table of Contents: -
 Rev. Type: Peer
 Identifiers: eDoc: 300557
ISI: 000238804400010
ISI: 000238804400010
DOI: 10.1523/JNEUROSCI.1013-06.2006
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Title: Journal of Neuroscience
  Alternative Title : J Neurosci
Source Genre: Journal
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Pages: - Volume / Issue: 26 (26) Sequence Number: - Start / End Page: 6968 - 6978 Identifier: ISSN: 0270-6474