Suppr超能文献

内嗅皮层损伤后大鼠齿状回中含小白蛋白神经元输入突触的重组

Reorganization of input synapses of parvalbumin-containing neurons in the rat fascia dentata following entorhinal lesion.

作者信息

Nitsch R, Bader S, Frotscher M

机构信息

Institute of Anatomy, University of Freiburg, F.R.G.

出版信息

Neurosci Lett. 1992 Jan 20;135(1):33-6. doi: 10.1016/0304-3940(92)90129-u.

Abstract

Removal of ipsilateral entorhinal afferents to the fascia dentata results in a retraction of postsynaptic parvalbumin (PARV)-containing dendrites of GABAergic neurons from the outer molecular layer. This study analyzes the reorganization of input synapses of these identified neurons following deafferentation. The density of synaptic input (total length of synaptic membrane specializations) of PARV-immunostained dendrites increased by 34% in the outer molecular layer of the fascia dentata 8 days, and by 21% 55 days following lesion when compared with unoperated controls. Eight days postlesion this increase was mainly due to an enlargement of synaptic membrane specializations of single terminals whereas 55 days after the lesion there was an increase in the number of synapses on the identified dendrites. Our results suggest expansion of terminals of remaining afferent systems (i.e. commissural fibers) in the early postlesional period and reactive synaptogenesis (i.e. de novo formation of synaptic contacts) on PARV-positive dendrites after long survival time. This increased innervation may be of functional importance as it might compensate for the reduction of the receptive field of the PARV-positive, supposedly inhibitory neurons in the postlesional dentate gyrus.

摘要

切除齿状回同侧内嗅传入纤维会导致来自外分子层的含小白蛋白(PARV)的GABA能神经元的突触后树突回缩。本研究分析了去传入神经后这些已识别神经元的输入突触的重组情况。与未手术的对照组相比,在损伤后8天,齿状回外分子层中PARV免疫染色树突的突触输入密度(突触膜特化的总长度)增加了34%,在损伤后55天增加了21%。损伤后8天,这种增加主要是由于单个终末的突触膜特化增大,而损伤后55天,已识别树突上的突触数量增加。我们的结果表明,在损伤后的早期,剩余传入系统(即连合纤维)的终末会扩张,而在长时间存活后,PARV阳性树突上会发生反应性突触形成(即突触接触的从头形成)。这种增加的神经支配可能具有功能重要性,因为它可能补偿损伤后齿状回中PARV阳性、推测为抑制性神经元的感受野的减少。

文献AI研究员

20分钟写一篇综述,助力文献阅读效率提升50倍。

立即体验

用中文搜PubMed

大模型驱动的PubMed中文搜索引擎

马上搜索

文档翻译

学术文献翻译模型,支持多种主流文档格式。

立即体验