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EFA6A是一种针对Arf6的鸟嘌呤核苷酸交换因子,它在海马体中调控与发育阶段相关的棘突形态发生、突触可塑性和长期记忆。

EFA6A, a Guanine Nucleotide Exchange Factor for Arf6, Regulates Developmental Stage-Dependent Spine Morphogenesis, Synaptic Plasticity, and Long-Term Memory in the Hippocampus.

作者信息

Sugawara Takeyuki, Matsu-Ura Hikaru, Inagaki Ryo, Kawamura Taichi, Tanaka Manabu, Hara Yoshinobu, Saito Koji, Fukaya Masahiro, Moriguchi Shigeki, Sakagami Hiroyuki

机构信息

Department of Anatomy, Kitasato University School of Medicine, 1-15-1 Kitazato, Minami-ku, Sagamihara, Kanagawa, 252-0374, Japan.

Research Center for Pharmaceutical Development, Graduate School of Pharmaceutical Sciences, Tohoku University, 6-3 Aramaki-Aoba, Aoba-ku, Sendai, Miyagi, 980-8578, Japan.

出版信息

Mol Neurobiol. 2025 May 8. doi: 10.1007/s12035-025-05009-x.

Abstract

EFA6A is a guanine nucleotide exchange factor for ADP ribosylation factor 6 (Arf6), a small GTPase involved in membrane trafficking and actin cytoskeleton remodeling. While EFA6A-Arf6 signaling has been shown to regulate dendritic spine formation and maintenance in cultured neurons, its role in higher brain functions remains unclear in vivo. Here, we generated mice lacking two EFA6A splicing isoforms, EFA6A and EFA6As, to examine their role in regulating spine morphology and hippocampus-dependent learning and memory. The loss of EFA6A and EFA6As caused reduced dendritic spine density in developing CA1 pyramidal neurons, whereas dendritic spines aberrantly increased in adults. Furthermore, the mutant mice also showed impaired maintenance of long-term potentiation (LTP) at Schaffer collateral-CA1 synapses in the hippocampus and memory retention in the passive avoidance test. These findings provide the first in vivo evidence that the EFA6A isoforms, EFA6A and EFA6As, collectively regulate spine formation bidirectionally in a developmental stage-dependent manner, which is likely to underlie hippocampal synaptic plasticity and memory formation.

摘要

EFA6A是一种针对ADP核糖基化因子6(Arf6)的鸟嘌呤核苷酸交换因子,Arf6是一种参与膜运输和肌动蛋白细胞骨架重塑的小GTP酶。虽然EFA6A-Arf6信号通路已被证明可调节培养神经元中树突棘的形成和维持,但其在体内高等脑功能中的作用仍不清楚。在这里,我们生成了缺乏两种EFA6A剪接异构体EFA6A和EFA6As的小鼠,以研究它们在调节脊柱形态以及海马体依赖性学习和记忆中的作用。EFA6A和EFA6As的缺失导致发育中的CA1锥体神经元树突棘密度降低,而在成年小鼠中树突棘异常增加。此外,突变小鼠在海马体中Schaffer侧支-CA1突触处的长期增强(LTP)维持能力也受损,并且在被动回避试验中的记忆保持能力也受损。这些发现首次提供了体内证据,表明EFA6A异构体EFA6A和EFA6As以发育阶段依赖性方式共同双向调节脊柱形成,这可能是海马体突触可塑性和记忆形成的基础。

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