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利用原子力显微镜研究体外神经突与肥大细胞(RBL)的直接通讯。

Atomic force microscopy to study direct neurite-mast cell (RBL) communication in vitro.

作者信息

Ohshiro H, Suzuki R, Furuno T, Nakanishi M

机构信息

Faculty of Pharmaceutical Sciences, Nagoya City University, Tanabe-dori, Mizuho-ku, 467-8603, Nagoya, Japan.

出版信息

Immunol Lett. 2000 Nov 1;74(3):211-4. doi: 10.1016/s0165-2478(00)00211-x.

Abstract

Communication between nerves and mast cells is a prototypic demonstration of neuroimmune interaction. We used an in vitro co-culture approach comprising cultured murine superior cervical ganglia (SCG) and rat basophilic leukemia (RBL-2H3) cells. Atomic force microscopy (AFM) showed how neurites attached to a pseudopodium or a cell body of an RBL cell. After stimulation of SCG neurites with bradykinin or scorpion venom, RBL cells attached to neurites spread and flattened, and several discharged granules (0. 5-1.0 microm in diameter) were found on the surface of the RBL cells. A neurokinin (NK)-1 receptor (i.e. substance P receptor) antagonist prevented the RBL degranulation. The results showed that activation of the SCG neurites with bradykinin or scorpion venom was able to elicit degranulation in RBL cells which were attached to neurites.

摘要

神经与肥大细胞之间的通讯是神经免疫相互作用的典型例证。我们采用了一种体外共培养方法,即将培养的小鼠颈上神经节(SCG)与大鼠嗜碱性白血病(RBL-2H3)细胞进行共培养。原子力显微镜(AFM)显示了神经突如何附着于RBL细胞的伪足或细胞体上。用缓激肽或蝎毒刺激SCG神经突后,附着于神经突的RBL细胞会伸展并变平,并且在RBL细胞表面发现了几个排出的颗粒(直径0.5 - 1.0微米)。一种神经激肽(NK)-1受体(即P物质受体)拮抗剂可阻止RBL细胞脱颗粒。结果表明,用缓激肽或蝎毒激活SCG神经突能够引发附着于神经突的RBL细胞脱颗粒。

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