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新生大鼠轻度缺氧后rab 3A和突触小泡蛋白免疫反应性的短暂增加。

Transient increase in rab 3A and synaptobrevin immunoreactivity after mild hypoxia in neonatal rats.

作者信息

Manzur A, Sosa M, Seltzer A M

机构信息

Instituto de Histología y Embriología, Facultad de Ciencias Médicas, Universidad Nacional de Cuyo, Mendoza, Argentina.

出版信息

Cell Mol Neurobiol. 2001 Feb;21(1):39-52. doi: 10.1023/a:1007169228329.

Abstract
  1. In the present work we describe the short term effects of mild neonatal hypoxia on the synapse as assessed by the immunoreactivity (IR) of two synaptic proteins: rab 3A and synaptobrevin (VAMP). 2. Using the sensitive methodology of immunoblotting, we measured rab 3A and VAMP-IR in homogenates from the cerebral cortex, hippocampus, and corpus striatum of control (breathing room air) and hypoxiated (breathing 95.5% N2-6.5% O2 for 70 min) 4-day-old rats at 1, 2, and 6 h after the end of the hypoxia. Immunostaining with examination by light microscopy was performed using the synaptic protein-specific antibodies on fixed brain sections from animals belonging to the same litter and submitted to hypoxia. 3. A transient increase of VAMP-IR was observed in the hippocampus and corpus striatum, and for rab 3A in the striatum, 1 h after initiating reoxygenation. At the following time points the values returned to control levels. This effect was less clearly observed in the immunostained sections. 4. Mild hypoxia has an effect on sensitive brain regions, eliciting an increase in the IR of at least two proteins involved in the synaptic vesicle cycle. The transient nature of this effect possibly indicates the activation of endogenous neuroprotective mechanisms.
摘要
  1. 在本研究中,我们描述了轻度新生儿缺氧对突触的短期影响,该影响通过两种突触蛋白:rab 3A和突触囊泡蛋白(VAMP)的免疫反应性(IR)进行评估。2. 使用免疫印迹的灵敏方法,我们在缺氧结束后1小时、2小时和6小时,测量了对照组(呼吸室内空气)和缺氧组(呼吸95.5% N₂ - 6.5% O₂ 70分钟)4日龄大鼠大脑皮质、海马体和纹状体匀浆中的rab 3A和VAMP-IR。使用突触蛋白特异性抗体对来自同一窝且经历缺氧的动物的固定脑切片进行免疫染色,并通过光学显微镜检查。3. 在复氧开始1小时后,观察到海马体和纹状体中VAMP-IR短暂增加,纹状体中rab 3A也短暂增加。在随后的时间点,这些值恢复到对照水平。在免疫染色切片中这种效应不太明显。4. 轻度缺氧对敏感脑区有影响,引发参与突触小泡循环的至少两种蛋白质的IR增加。这种效应的短暂性质可能表明内源性神经保护机制的激活。

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