N-cadherin, spine dynamics, and synaptic function

Mysore, S. P.; Tai, C. Y.; Schuman, Erin M.

doi:10.3389/neuro.01.035.2008

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N-cadherin, spine dynamics, and synaptic function

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Schuman, Erin M.
Synaptic Plasticity Department, Max Planck Institute for Brain Research, Max Planck Society;

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https://www.ncbi.nlm.nih.gov/pubmed/19225589
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Mysore, S. P., Tai, C. Y., & Schuman, E. M. (2009). N-cadherin, spine dynamics, and synaptic function. Front Neurosci, 2(2), 168-75.

Cite as: https://hdl.handle.net/21.11116/0000-0007-EF3A-C

Abstract

Dendritic spines are one-half (the postsynaptic half) of most excitatory synapses. Ever since the direct observation over a decade ago that spines can continually change size and shape, spine dynamics has been of great research interest, especially as a mechanism for structural synaptic plasticity. In concert with this ongoing spine dynamics, the stability of the synapse is also needed to allow continued, reliable synaptic communication. Various cell-adhesion molecules help to structurally stabilize a synapse and its proteins. Here, we review the effects of disrupting N-cadherin, a prominent trans-synaptic adhesion molecule, on spine dynamics, as reported in Mysore et al. (2007). We highlight the novel method adopted therein to reliably detect even subtle changes in fast and slow spine dynamics. We summarize the structural, functional, and molecular consequences of acute N-cadherin disruption, and tie them in, in a working model, with longer-term effects on spines and synapses reported in the literature.