Loss of Cdc42 leads to defects in synaptic plasticity and remote memory recall.

Published online

Journal Article

Cdc42 is a signaling protein important for reorganization of actin cytoskeleton and morphogenesis of cells. However, the functional role of Cdc42 in synaptic plasticity and in behaviors such as learning and memory are not well understood. Here we report that postnatal forebrain deletion of Cdc42 leads to deficits in synaptic plasticity and in remote memory recall using conditional knockout of Cdc42. We found that deletion of Cdc42 impaired LTP in the Schaffer collateral synapses and postsynaptic structural plasticity of dendritic spines in CA1 pyramidal neurons in the hippocampus. Additionally, loss of Cdc42 did not affect memory acquisition, but instead significantly impaired remote memory recall. Together these results indicate that the postnatal functions of Cdc42 may be crucial for the synaptic plasticity in hippocampal neurons, which contribute to the capacity for remote memory recall.

Full Text

Duke Authors

Cited Authors

  • Kim, IH; Wang, H; Soderling, SH; Yasuda, R

Published Date

  • July 8, 2014

Published In

Volume / Issue

  • 3 /

PubMed ID

  • 25006034

Pubmed Central ID

  • 25006034

Electronic International Standard Serial Number (EISSN)

  • 2050-084X

Digital Object Identifier (DOI)

  • 10.7554/eLife.02839

Language

  • eng

Conference Location

  • England