Loss of Cdc42 leads to defects in synaptic plasticity and remote memory recall
- Duke University Medical School, United States
- Max Planck Florida Institute, United States
Abstract
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 the 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.
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Author details
Reviewing Editor
- Eunjoon Kim, Korea Advanced Institute of Science and Technology, South Korea
Ethics
Animal experimentation: The institutional animal care and use committee (IACUC) of the Duke University Medical Center and the approved animal protocols are A113-11-05 and A288-11-11. The institutional guidelines for the care and use of laboratory animals were followed.
Version history
- Received: March 19, 2014
- Accepted: July 6, 2014
- Accepted Manuscript published: July 8, 2014 (version 1)
- Version of Record published: August 1, 2014 (version 2)
Copyright
This is an open-access article, free of all copyright, and may be freely reproduced, distributed, transmitted, modified, built upon, or otherwise used by anyone for any lawful purpose. The work is made available under the Creative Commons CC0 public domain dedication.
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Loss of Cdc42 leads to defects in synaptic plasticity and remote memory recall
eLife 3:e02839.
https://doi.org/10.7554/eLife.02839
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