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DIP/WISH 缺乏增强了巴恩斯迷宫中的突触功能和表现。

DIP/WISH deficiency enhances synaptic function and performance in the Barnes maze.

机构信息

Division of Cell Signaling, Okazaki Institute for Integrative Bioscience (National Institute for Physiological Sciences), Japan.

出版信息

Mol Brain. 2011 Oct 21;4:39. doi: 10.1186/1756-6606-4-39.

DOI:10.1186/1756-6606-4-39
PMID:22018352
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3208581/
Abstract

BACKGROUND

DIP (diaphanous interacting protein)/WISH (WASP interacting SH3 protein) is a protein involved in cytoskeletal signaling which regulates actin cytoskeleton dynamics and/or microtubules mainly through the activity of Rho-related proteins. Although it is well established that: 1) spine-head volumes change dynamically and reflect the strength of the synapse accompanying long-term functional plasticity of glutamatergic synaptic transmission and 2) actin organization is critically involved in spine formation, the involvement of DIP/WISH in these processes is unknown.

RESULTS

We found that DIP/WISH-deficient hippocampal CA1 neurons exhibit enhanced long-term potentiation via modulation of both pre- and post-synaptic events. Consistent with these electrophysiological findings, DIP/WISH-deficient mice, particularly at a relatively young age, found the escape hole more rapidly in the Barnes maze test.

CONCLUSIONS

We conclude that DIP/WISH deletion improves performance in the Barnes maze test in mice probably through increased hippocampal long-term potentiation.

摘要

背景

DIP（透化蛋白）/WISH（WASP 相互作用 SH3 蛋白）是一种参与细胞骨架信号转导的蛋白质，主要通过 Rho 相关蛋白的活性调节肌动蛋白细胞骨架动力学和/或微管。尽管已经确定：1）棘突头部体积动态变化，反映伴随谷氨酸能突触传递的长期功能可塑性的突触强度，2）肌动蛋白组织在棘突形成中起关键作用，但 DIP/WISH 在这些过程中的参与尚不清楚。

结果

我们发现 DIP/WISH 缺陷型海马 CA1 神经元通过调节突触前和突触后事件表现出增强的长时程增强。与这些电生理发现一致，DIP/WISH 缺陷型小鼠，特别是在相对年轻的时候，在 Barnes 迷宫测试中更快地找到了逃生洞。

结论

我们得出结论，DIP/WISH 的缺失可能通过增加海马长时程增强来提高小鼠在 Barnes 迷宫测试中的表现。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4821/3208581/2ace0ed00b80/1756-6606-4-39-6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4821/3208581/2f90569ee70d/1756-6606-4-39-1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4821/3208581/233d7e6e0815/1756-6606-4-39-2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4821/3208581/aad701ff8bf9/1756-6606-4-39-3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4821/3208581/b941c8d8d3d2/1756-6606-4-39-4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4821/3208581/c19fedd5dbe1/1756-6606-4-39-5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4821/3208581/2ace0ed00b80/1756-6606-4-39-6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4821/3208581/2f90569ee70d/1756-6606-4-39-1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4821/3208581/233d7e6e0815/1756-6606-4-39-2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4821/3208581/aad701ff8bf9/1756-6606-4-39-3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4821/3208581/b941c8d8d3d2/1756-6606-4-39-4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4821/3208581/c19fedd5dbe1/1756-6606-4-39-5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4821/3208581/2ace0ed00b80/1756-6606-4-39-6.jpg

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