Kim Il Hwan, Wang Hong, Soderling Scott H, Yasuda Ryohei
Department of Cell Biology, Duke University Medical School, Durham, United States.
Department of Neurobiology, Duke University Medical School, Durham, United States.
Elife. 2014 Jul 8;3:e02839. doi: 10.7554/eLife.02839.
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.
Cdc42是一种信号蛋白，对肌动蛋白细胞骨架的重组和细胞形态发生很重要。然而，Cdc42在突触可塑性以及学习和记忆等行为中的功能作用尚未得到充分了解。在这里，我们报告说，使用Cdc42条件性敲除，出生后前脑Cdc42缺失会导致突触可塑性和远程记忆回忆出现缺陷。我们发现，Cdc42的缺失损害了海马体中CA1锥体神经元的Schaffer侧支突触中的长时程增强（LTP）以及树突棘的突触后结构可塑性。此外，Cdc42的缺失不影响记忆获取，但会显著损害远程记忆回忆。这些结果共同表明，Cdc42的出生后功能可能对海马神经元的突触可塑性至关重要，而突触可塑性有助于远程记忆回忆的能力。
