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β1肾上腺素能受体在耳蜗和前庭迷路中的定位。

Localization of beta1-adrenergic receptors in the cochlea and the vestibular labyrinth.

作者信息

Fauser C, Schimanski S, Wangemann P

机构信息

Cell Physiology Laboratory, Anatomy & Physiology Department, Kansas State University, Manhattan, KS 66506, USA.

出版信息

J Membr Biol. 2004 Sep 1;201(1):25-32. doi: 10.1007/s00232-004-0703-x.

DOI:10.1007/s00232-004-0703-x
PMID:15635809
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2020520/
Abstract

Sympathetic activation in a "fight or flight reaction" may put the sensory systems for hearing and balance into a state of heightened alert via beta1-adrenergic receptors (beta1-AR). The aim of the present study was to localize beta1-AR in the gerbil inner ear by confocal immunocytochemistry, to characterize beta1-AR by Western immunoblots, and to identify beta1-AR pharmacologically by measurements of cAMP production. Staining for beta1-AR was found in strial marginal cells, inner and outer hair cells, outer sulcus, and spiral ganglia cells of the cochlea, as well as in dark, transitional and supporting cells of the vestibular labyrinth. Receptors were characterized in microdissected inner ear tissue fractions as 55 kDa non-glycosylated species and as 160 kDa high-mannose-glycosylated complexes. Pharmacological studies using isoproterenol, ICI-118551 and CGP-20712A demonstrated beta1-AR as the predominant adrenergic receptor in stria vascularis and organ of Corti. In conclusion, beta1-AR are present and functional in inner ear epithelial cells that are involved in K+ cycling and auditory transduction, as well as in neuronal cells that are involved in auditory transmission.

摘要

“战斗或逃跑反应”中的交感神经激活可能通过β1-肾上腺素能受体(β1-AR)使听觉和平衡感觉系统进入高度警觉状态。本研究的目的是通过共聚焦免疫细胞化学在沙鼠内耳中定位β1-AR,通过蛋白质免疫印迹法对β1-AR进行表征,并通过测量环磷酸腺苷(cAMP)生成从药理学角度鉴定β1-AR。在血管纹边缘细胞、内外毛细胞、外沟以及耳蜗螺旋神经节细胞中发现了β1-AR染色,在前庭迷路的暗细胞、过渡细胞和支持细胞中也有发现。在内耳组织微切割部分中,受体被表征为55 kDa的非糖基化物种和160 kDa的高甘露糖糖基化复合物。使用异丙肾上腺素、ICI-118551和CGP-20712A进行的药理学研究表明,β1-AR是血管纹和柯蒂氏器中主要的肾上腺素能受体。总之,β1-AR存在于参与钾离子循环和听觉转导的内耳上皮细胞以及参与听觉传导的神经元细胞中并发挥作用。

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本文引用的文献

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Chloride secretion by semicircular canal duct epithelium is stimulated via beta 2-adrenergic receptors.
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