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神经介素缺陷小鼠海马体中突触和神经元的异常。

Abnormalities of synapses and neurons in the hippocampus of neuropsin-deficient mice.

作者信息

Hirata A, Yoshida S, Inoue N, Matsumoto-Miyai K, Ninomiya A, Taniguchi M, Matsuyama T, Kato K, Iizasa H, Kataoka Y, Yoshida N, Shiosaka S

机构信息

Division of Structural Cell Biology, Nara Institute of Science and Technology (NAIST), Nara.

出版信息

Mol Cell Neurosci. 2001 Mar;17(3):600-10. doi: 10.1006/mcne.2000.0945.

DOI:10.1006/mcne.2000.0945
PMID:11273653
Abstract

In the present study, we produced null-mutant mice of neuropsin, an extracellular matrix serine protease, to examine the neural functions of this protein particularly in the hippocampus. Golgi-Cox impregnation and Nissl-staining revealed morphological change of cell soma in the mutant mice compared to wild-type mice. However, Golgi-Cox impregnation revealed no apparent change in the dendritic arborization and spine density. Quantitative electronmicroscopic analysis revealed that number of asymmetrical synapses were significantly decreased in the stratum radiatum, the major terminal field of Schaffer-collaterals, whereas free boutons still holding synaptic vesicles but with no synaptic specialization were increased in number in the same microscopic fields. An increased number of parvalbumin-immunoreactive cells (known as fast spiking cells) in mutant was also observed. These results strongly suggest that neuropsin is involved in connectivity of a group of CA1 synapses and consequently in the hippocampal networking.

摘要

在本研究中,我们培育了细胞外基质丝氨酸蛋白酶神经胰蛋白酶的基因敲除小鼠,以研究该蛋白的神经功能,特别是在海马体中的功能。高尔基-考克斯染色法和尼氏染色法显示,与野生型小鼠相比,突变小鼠的细胞体形态发生了变化。然而,高尔基-考克斯染色法显示树突分支和棘密度没有明显变化。定量电子显微镜分析显示,在放射层(沙费尔侧支的主要终末区域),不对称突触的数量显著减少,而在相同显微镜视野中,仍含有突触小泡但无突触特化的游离终扣数量增加。在突变体中还观察到小清蛋白免疫反应性细胞(即快速放电细胞)数量增加。这些结果有力地表明,神经胰蛋白酶参与了一组CA1突触的连接,进而参与了海马体网络的形成。

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