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The Journal of Neuroscience, December 3, 2003, 23(35):11008-11014

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Cellular/Molecular
Ca²⁺ Dependency of N-Cadherin Function Probed by Laser Tweezer and Atomic Force Microscopy

Werner Baumgartner, ^* Nikola Golenhofen, ^* Niko Grundhöfer, Johannes Wiegand, and Detlev Drenckhahn

Institute of Anatomy and Cell Biology, University of Würzburg, D-97070 Würzburg, Germany

This study was undertaken to provide a biophysical basis for the hypothesis that activity-dependent modulation of cadherin-mediated adhesion by transient changes of extracellular calcium ([Ca²⁺]_e) is causally involved in coordination of synaptic plasticity. Characterization of homophilic N-cadherin binding by atomic force microscopy and laser tweezer trapping of N-cadherin-coated microbeads attached to the cell surface of cultured neuronal cells showed that adhesive activity of N-cadherin is effectively regulated between 0.3 and 0.8 mM [Ca²⁺]_e. Furthermore, we show that an increase of [Ca²⁺]_i, which is known to be essential for induction of synaptic plasticity, causes significant reduction of cadherin-mediated bead adhesion that could be completely suppressed by inhibition of actin depolymerization. The results of this study show that N-cadherin has ideal biophysical properties to serve as a Ca²⁺-dependent sensor for synaptic activity and, at the same time, is strategically located to control synaptic adhesion. A drop of [Ca²⁺]_e and a concomitant increase of [Ca²⁺]_i may act in concert to modulate N-cadherin-based adhesive contacts at synaptic sites.

Key words: synaptic plasticity; long-term potentiation; actin; PC12 cells; cadherin 2; VE-cadherin

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Received April 30, 2003; revised September 22, 2003; accepted October 6, 2003.

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