Synaptic Homeostasis and Input Selectivity Follow From a Calcium-Dependent Plasticity Model.

Luk Chong Yeung, Brown University
Harel Z. Shouval, Brown University
Brian S. Blais, Bryant University
Leon N. Cooper, Brown University

Document Type Article

Published by The National Academy of Sciences of the United States of America in: Proceedings of the National Academy of Sciences of the United States of America. Volume 101, issue 41, 2004, Pages 14943–14948
Available at PNAS
or Pubmed


Modifications in the strengths of synapses are thought to underlie memory, learning, and development of cortical circuits. Many cellular mechanisms of synaptic plasticity have been investigated in which differential elevations of postsynaptic calcium concentrations play a key role in determining the direction and magnitude of synaptic changes. We have previously described a model of plasticity that uses calcium currents mediated by N-methyl-d-aspartate receptors as the associative signal for Hebbian learning. However, this model is not completely stable. Here, we propose a mechanism of stabilization through homeostatic regulation of intracellular calcium levels. With this model, synapses are stable and exhibit properties such as those observed in metaplasticity and synaptic scaling. In addition, the model displays synaptic competition, allowing structures to emerge in the synaptic space that reflect the statistical properties of the inputs. Therefore, the combination of a fast calcium-dependent learning and a slow stabilization mechanism can account for both the formation of selective receptive fields and the maintenance of neural circuits in a state of equilibrium.