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血清素诱导外源性过氧化物酶跨脑血管的囊泡转运增强。

Enhanced vesicular transport of exogenous peroxidase across cerebral vessels, induced by serotonin.

作者信息

Westergaard E

出版信息

Acta Neuropathol. 1975;32(1):27-42. doi: 10.1007/BF00686065.

Abstract

Previous studies have revealed that the endothelial cells of cerebral vessels are linked by tight junctions preventing an intercellular passage of exogenous peroxidase. However, under normal conditions, vesicular transport of the tracer has been demonstrated in parts of cerebral vessels, especially in arterioles with a diameter of 30-100 mu. Solutions, containing 50-800 mug of buffered 5-hydroxytryptamine sulphate (serotonin), were perfused through the cerebral ventricles on mice after intravenous injection of horseradish peroxidase. Usually, the biogenic amine enhanced the vesicular transport of exogenous peroxidase. The serotonin-induced increased transport was observed in vessels on the surface of the brain as well as in vessels located in the parenchyma. No cell damage was observed. Increased transport was observed in arterioles, venules, and in capillaries. Therefore, it is not likely that the serotonin effect is a constriction of smooth muscle cells causing an opening of the tight junctions followed by an intercellular movement of tracer. The most reasonable assumption behind the mechanism is that serotonin affects the plasmamembrane of endothelial cells resulting in an enhanced production and transfer of cytoplasmic vesicles.

摘要

先前的研究表明,脑血管内皮细胞通过紧密连接相连,可阻止外源性过氧化物酶在细胞间通过。然而,在正常情况下,已证实在部分脑血管中存在示踪剂的囊泡运输,尤其是在直径为30 - 100微米的小动脉中。在静脉注射辣根过氧化物酶后,将含有50 - 800微克缓冲硫酸5 - 羟色胺(血清素)的溶液灌注到小鼠脑室中。通常,生物胺会增强外源性过氧化物酶的囊泡运输。在脑表面的血管以及实质内的血管中均观察到血清素诱导的运输增加。未观察到细胞损伤。在小动脉、小静脉和毛细血管中均观察到运输增加。因此,血清素的作用不太可能是通过收缩平滑肌细胞导致紧密连接开放,进而使示踪剂在细胞间移动。该机制背后最合理的假设是,血清素影响内皮细胞的质膜,导致细胞质囊泡的产生和转运增强。

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