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NELL2基因缺陷小鼠齿状回体内长时程增强作用增强。

Enhanced long-term potentiation in vivo in dentate gyrus of NELL2-deficient mice.

作者信息

Matsuyama Shogo, Aihara Koutoku, Nishino Naoki, Takeda Satoshi, Tanizawa Katsuyuki, Kuroda Shun'ichi, Horie Masato

机构信息

Division of Molecular Pharmacology and Pharmacogenomics, Department of Genome Sciences, Kobe University Graduate School of Medicine, Hyogo 650-0017, Japan.

出版信息

Neuroreport. 2004 Mar 1;15(3):417-20. doi: 10.1097/00001756-200403010-00007.

Abstract

NELL2 is a neuron-specific thrombospondin-1-like extracellular protein containing six epidermal growth factor-like domains and is highly expressed in the hippocampus. We have previously shown that NELL2 promotes survival of neurons through mitogen-activated protein kinases. To clarify the function of NELL2 in vivo, we have generated a novel strain of mice with a targeted mutation in the NELL2 gene and assessed long-term potentiation (LTP) in vivo in the dentate gyrus of NELL2-deficient mice using extracellular recording techniques. Production of LTP at perforant path-granule cell synapses was significantly larger in NELL2-deficient mice than in wild-type controls. Thus, we propose that NELL2 plays an important role as a novel suppressor in LTP in vivo in the mouse dentate gyrus.

摘要

NELL2是一种神经元特异性的血小板反应蛋白-1样细胞外蛋白,含有六个表皮生长因子样结构域,在海马体中高度表达。我们之前已经表明,NELL2通过丝裂原活化蛋白激酶促进神经元存活。为了阐明NELL2在体内的功能,我们构建了一种新型的小鼠品系,其NELL2基因发生了靶向突变,并使用细胞外记录技术在NELL2缺陷小鼠的齿状回中评估了体内长时程增强(LTP)。在穿孔通路-颗粒细胞突触处,NELL2缺陷小鼠的LTP产生明显大于野生型对照。因此,我们提出NELL2作为一种新型抑制因子在小鼠齿状回的体内LTP中起重要作用。

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