被迫的神经元相互作用导致沟通不良。

Neurogenesis (Austin, Tex.) Pub Date : 2017-02-06 eCollection Date: 2017-01-01 DOI:10.1080/23262133.2017.1286424
Marine Krzisch, Nicolas Toni
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引用次数: 0

摘要

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。

Forced neuronal interactions cause poor communication.

Forced neuronal interactions cause poor communication.

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.

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