Forced neuronal interactions cause poor communication.

Neurogenesis (Austin, Tex.) Pub Date : 2017-02-06 eCollection Date: 2017-01-01 DOI:10.1080/23262133.2017.1286424
Marine Krzisch, Nicolas Toni
{"title":"Forced neuronal interactions cause poor communication.","authors":"Marine Krzisch,&nbsp;Nicolas Toni","doi":"10.1080/23262133.2017.1286424","DOIUrl":null,"url":null,"abstract":"<p><p>Post-natal hippocampal neurogenesis plays a role in hippocampal function, and neurons born post-natally participate to spatial memory and mood control. However, a great proportion of granule neurons generated in the post-natal hippocampus are eliminated during the first 3 weeks of their maturation, a mechanism that depends on their synaptic integration. In a recent study, we examined the possibility of enhancing the synaptic integration of neurons born post-natally, by specifically overexpressing synaptic cell adhesion molecules in these cells. Synaptic cell adhesion molecules are transmembrane proteins mediating the physical connection between pre- and post-synaptic neurons at the synapse, and their overexpression enhances synapse formation. Accordingly, we found that overexpressing synaptic adhesion molecules increased the synaptic integration and survival of newborn neurons. Surprisingly, the synaptic adhesion molecule with the strongest effect on new neurons' survival, Neuroligin-2A, decreased memory performances in a water maze task. We present here hypotheses explaining these surprising results, in the light of the current knowledge of the mechanisms of synaptic integration of new neurons in the post-natal hippocampus.</p>","PeriodicalId":74274,"journal":{"name":"Neurogenesis (Austin, Tex.)","volume":null,"pages":null},"PeriodicalIF":0.0000,"publicationDate":"2017-02-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/23262133.2017.1286424","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Neurogenesis (Austin, Tex.)","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.1080/23262133.2017.1286424","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2017/1/1 0:00:00","PubModel":"eCollection","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 0

Abstract

Post-natal hippocampal neurogenesis plays a role in hippocampal function, and neurons born post-natally participate to spatial memory and mood control. However, a great proportion of granule neurons generated in the post-natal hippocampus are eliminated during the first 3 weeks of their maturation, a mechanism that depends on their synaptic integration. In a recent study, we examined the possibility of enhancing the synaptic integration of neurons born post-natally, by specifically overexpressing synaptic cell adhesion molecules in these cells. Synaptic cell adhesion molecules are transmembrane proteins mediating the physical connection between pre- and post-synaptic neurons at the synapse, and their overexpression enhances synapse formation. Accordingly, we found that overexpressing synaptic adhesion molecules increased the synaptic integration and survival of newborn neurons. Surprisingly, the synaptic adhesion molecule with the strongest effect on new neurons' survival, Neuroligin-2A, decreased memory performances in a water maze task. We present here hypotheses explaining these surprising results, in the light of the current knowledge of the mechanisms of synaptic integration of new neurons in the post-natal hippocampus.

Abstract Image

被迫的神经元相互作用导致沟通不良。
出生后的海马神经发生在海马功能中起作用,出生后的神经元参与空间记忆和情绪控制。然而,出生后海马中产生的很大一部分颗粒神经元在其成熟的前3周内被消除,这一机制取决于它们的突触整合。在最近的一项研究中,我们研究了通过在这些细胞中特异性地过表达突触细胞粘附分子来增强后天出生的神经元突触整合的可能性。突触细胞粘附分子是一种跨膜蛋白,介导突触前和突触后神经元之间的物理连接,其过表达促进突触的形成。因此,我们发现突触粘附分子的过表达增加了新生神经元的突触整合和存活。令人惊讶的是,对新神经元存活影响最大的突触粘附分子Neuroligin-2A在水迷宫任务中降低了记忆表现。根据目前对出生后海马中新神经元突触整合机制的了解,我们提出了解释这些惊人结果的假设。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
求助全文
约1分钟内获得全文 求助全文
来源期刊
自引率
0.00%
发文量
0
×
引用
GB/T 7714-2015
复制
MLA
复制
APA
复制
导出至
BibTeX EndNote RefMan NoteFirst NoteExpress
×
提示
您的信息不完整,为了账户安全,请先补充。
现在去补充
×
提示
您因"违规操作"
具体请查看互助需知
我知道了
×
提示
确定
请完成安全验证×
copy
已复制链接
快去分享给好友吧!
我知道了
右上角分享
点击右上角分享
0
联系我们:info@booksci.cn Book学术提供免费学术资源搜索服务,方便国内外学者检索中英文文献。致力于提供最便捷和优质的服务体验。 Copyright © 2023 布克学术 All rights reserved.
京ICP备2023020795号-1
ghs 京公网安备 11010802042870号
Book学术文献互助
Book学术文献互助群
群 号:481959085
Book学术官方微信