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Rho鸟嘌呤核苷酸交换因子4(Arhgef4)缺乏增强空间和物体识别记忆。

Rho Guanine Nucleotide Exchange Factor 4 (Arhgef4) Deficiency Enhances Spatial and Object Recognition Memory.

作者信息

Yoo Ki-Seo, Lee Kina, Lee Yong-Seok, Oh Won-Jong, Kim Hyong Kyu

机构信息

Department of Medicine and Microbiology, Graduate Program in Neuroscience, College of Medicine, Chungbuk National University, Cheongju 28644, Korea.

Department of Physiology, Department of Biomedical Science, Seoul National University College of Medicine, Seoul 03080, Korea.

出版信息

Exp Neurobiol. 2020 Oct 31;29(5):334-343. doi: 10.5607/en20049.

DOI:10.5607/en20049
PMID:33154196
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7649087/
Abstract

Guanine nucleotide exchange factors (GEFs) play multiple functional roles in neurons. In a previous study, we reported that (Rho guanine nucleotide exchange factor 4) functioned as a negative regulator of the excitatory synaptic function by sequestering postsynaptic density protein 95 (PSD-95). However, the role of in behavior has not been examined. We performed comprehensive behavioral tests in knockout (KO) mice to investigate of the effects of deficiency. We found that the expressed PSD-95 particle size was significantly increased in hippocampal neuronal cultures from KO mice, which is consistent with the previous findings. KO mice exhibited general motor activity and anxiety-like behavior comparable to those of the wild type littermates. However, spatial memory and object recognition memory were significantly enhanced in the KO mice. Taken together, these data confirm the role of as a negative synaptic regulator at the behavioral level.

摘要

鸟嘌呤核苷酸交换因子(GEFs)在神经元中发挥多种功能作用。在先前的一项研究中,我们报道了(Rho鸟嘌呤核苷酸交换因子4)通过隔离突触后致密蛋白95(PSD - 95)作为兴奋性突触功能的负调节因子。然而,其在行为中的作用尚未得到研究。我们在基因敲除(KO)小鼠中进行了全面的行为测试,以研究缺乏该因子的影响。我们发现,在来自基因敲除小鼠的海马神经元培养物中,表达的PSD - 95颗粒大小显著增加,这与之前的研究结果一致。基因敲除小鼠表现出与野生型同窝小鼠相当的一般运动活动和焦虑样行为。然而,基因敲除小鼠的空间记忆和物体识别记忆显著增强。综上所述,这些数据证实了该因子在行为水平上作为负突触调节因子的作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/678c/7649087/c7019c4bb9a6/EN-29-334-f4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/678c/7649087/3a69faca0100/EN-29-334-f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/678c/7649087/d7af8e330a41/EN-29-334-f2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/678c/7649087/77ebb69322d8/EN-29-334-f3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/678c/7649087/c7019c4bb9a6/EN-29-334-f4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/678c/7649087/3a69faca0100/EN-29-334-f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/678c/7649087/d7af8e330a41/EN-29-334-f2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/678c/7649087/77ebb69322d8/EN-29-334-f3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/678c/7649087/c7019c4bb9a6/EN-29-334-f4.jpg

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本文引用的文献

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Mol Brain. 2019 Nov 21;12(1):97. doi: 10.1186/s13041-019-0520-x.
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