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Differential control of presynaptic efficacy by postsynaptic N-cadherin and β-catenin. | LitMetric

Differential control of presynaptic efficacy by postsynaptic N-cadherin and β-catenin.

Nat Neurosci

Medical Research Council Laboratory for Molecular Cell Biology and Cell Biology Unit, University College London, London, UK.

Published: December 2011

AI Article Synopsis

  • - N-cadherin is a protein that helps neurons stick together at synapses and is important for maintaining synapse function in mature neurons beyond its initial role in their formation.
  • - Disrupting N-cadherin in postsynaptic neurons leads to decreased neurotransmitter release probabilities and affects how vesicles are recycled, indicating its critical role in synaptic transmission.
  • - While the loss of N-cadherin doesn’t stop the neuron from adjusting neurotransmitter release in response to chronic inactivity, removing β-catenin does hinder this ability, suggesting that different mechanisms govern baseline and adaptive changes in synaptic activity.

Article Abstract

N-cadherin is a homophilic adhesion protein that remains expressed at mature excitatory synapses beyond its developmental role in synapse formation. We investigated the trans-synaptic activity of N-cadherin in regulating synapse function in rodent cultured hippocampal neurons using optical methods and electrophysiology. Interfering with N-cadherin in postsynaptic neurons reduced basal release probability (p(r)) at inputs to the neuron, and this trans-synaptic impairment of release accompanied impaired vesicle endocytosis. Moreover, loss of the GluA2 AMPA-type glutamate receptor subunit, which decreased p(r) by itself, occluded the interference with postsynaptic N-cadherin. The loss of postsynaptic N-cadherin activity, however, did not affect the compensatory upregulation of p(r) induced by chronic activity silencing, whereas postsynaptic β-catenin deletion blocked this presynaptic homeostatic adaptation. Our findings suggest that postsynaptic N-cadherin helps link basal pre- and postsynaptic strengths to control the p(r) offset, whereas the p(r) gain adjustment requires a distinct trans-synaptic pathway involving β-catenin.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3245860PMC
http://dx.doi.org/10.1038/nn.2995DOI Listing

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