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齿状回中的突触可塑性和兴奋抑制平衡:神经连接蛋白-1、神经连接蛋白-2 和钙黏蛋白缺失敲除小鼠中的记录所提供的见解。

Synaptic Plasticity and Excitation-Inhibition Balance in the Dentate Gyrus: Insights from Recordings in Neuroligin-1, Neuroligin-2, and Collybistin Knockouts.

机构信息

Institute of Clinical Neuroanatomy, Neuroscience Center, Goethe University Frankfurt, Frankfurt, Germany.

Centre for the 3R-Principle, Faculty of Medicine, Justus Liebig University Giessen, Giessen, Germany.

出版信息

Neural Plast. 2018 Feb 18;2018:6015753. doi: 10.1155/2018/6015753. eCollection 2018.

Abstract

The hippocampal dentate gyrus plays a role in spatial learning and memory and is thought to encode differences between similar environments. The integrity of excitatory and inhibitory transmission and a fine balance between them is essential for efficient processing of information. Therefore, identification and functional characterization of crucial molecular players at excitatory and inhibitory inputs is critical for understanding the dentate gyrus function. In this minireview, we discuss recent studies unraveling molecular mechanisms of excitatory/inhibitory synaptic transmission, long-term synaptic plasticity, and dentate granule cell excitability in the hippocampus of live animals. We focus on the role of three major postsynaptic proteins localized at excitatory (neuroligin-1) and inhibitory synapses (neuroligin-2 and collybistin). recordings of field potentials have the advantage of characterizing the effects of the loss of these proteins on the input-output function of granule cells embedded in a network with intact connectivity. The lack of neuroligin-1 leads to deficient synaptic plasticity and reduced excitation but normal granule cell output, suggesting unaltered excitation-inhibition ratio. In contrast, the lack of neuroligin-2 and collybistin reduces inhibition resulting in a shift towards excitation of the dentate circuitry.

摘要

海马齿状回在空间学习和记忆中发挥作用,被认为可以对相似环境之间的差异进行编码。兴奋性和抑制性传递的完整性以及它们之间的精细平衡对于信息的有效处理至关重要。因此,识别和功能表征兴奋性和抑制性输入的关键分子参与者对于理解齿状回功能至关重要。在这篇综述中,我们讨论了最近的研究,这些研究揭示了活体内海马体中兴奋性/抑制性突触传递、长时程突触可塑性和颗粒细胞兴奋性的分子机制。我们重点介绍了三种主要的突触后蛋白在兴奋性(神经连接蛋白-1)和抑制性突触(神经连接蛋白-2 和 collybistin)中的作用。场电位记录具有的优势在于,可以表征这些蛋白缺失对嵌入具有完整连接性的网络中的颗粒细胞的输入-输出功能的影响。神经连接蛋白-1 的缺失导致突触可塑性不足和兴奋性降低,但颗粒细胞的输出正常,表明兴奋-抑制比不变。相比之下,神经连接蛋白-2 和 collybistin 的缺失减少了抑制作用,导致齿状回电路的兴奋转向。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4b2b/5835277/0b3da1771b2c/NP2018-6015753.001.jpg

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