Ca2+ dependency of N-cadherin function probed by laser tweezer and atomic force microscopy

J Neurosci. 2003 Dec 3;23(35):11008-14. doi: 10.1523/JNEUROSCI.23-35-11008.2003.

Abstract

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.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Actins / metabolism
  • Animals
  • Biophysical Phenomena
  • Biophysics
  • CHO Cells
  • Cadherins / metabolism*
  • Calcium / metabolism*
  • Cell Adhesion / physiology
  • Cell Line
  • Cricetinae
  • Humans
  • Lasers*
  • Microscopy, Atomic Force*
  • PC12 Cells
  • Rats

Substances

  • Actins
  • Cadherins
  • Calcium