de.mpg.escidoc.pubman.appbase.FacesBean
English
 
Help Guide Disclaimer Contact us Login
  Advanced SearchBrowse

Item

ITEM ACTIONSEXPORT

Released

Journal Article

Retrieval Property of Attractor Network with Synaptic Depression

MPS-Authors
http://pubman.mpdl.mpg.de/cone/persons/resource/persons84301

Ide D, Watanabe,  M
Department Physiology of Cognitive Processes, Max Planck Institute for Biological Cybernetics, Max Planck Society;

Locator
There are no locators available
Fulltext (public)
There are no public fulltexts available
Supplementary Material (public)
There is no public supplementary material available
Citation

Matsumoto, N., Ide D, Watanabe, M., & Okada, M. (2007). Retrieval Property of Attractor Network with Synaptic Depression. Journal of the Physical Society of Japan, 76(084005), 1-10. doi:10.1143/JPSJ.76.084005.


Cite as: http://hdl.handle.net/11858/00-001M-0000-0013-CF13-3
Abstract
Synaptic connections are known to change dynamically. High-frequency presynaptic inputs induce decrease of synaptic weights. This process is known as short-term synaptic depression. The synaptic depression controls a gain for presynaptic inputs. However, it remains a controversial issue what are functional roles of this gain control. We propose a new hypothesis that one of the functional roles is to enlarge basins of attraction. To verify this hypothesis, we employ a binary discrete-time associative memory model which consists of excitatory and inhibitory neurons. It is known that the excitatory–inhibitory balance controls an overall activity of the network. The synaptic depression might incorporate an activity control mechanism. Using a mean-field theory and computer simulations, we find that the synaptic depression enlarges the basins at a small loading rate while the excitatory–inhibitory balance enlarges them at a large loading rate. Furthermore the synaptic depression does not affect the steady state of the network if a threshold is set at an appropriate value. These results suggest that the synaptic depression works in addition to the effect of the excitatory–inhibitory balance, and it might improve an error-correcting ability in cortical circuits.