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在NG108 - 15细胞中,激动剂可迅速诱导125I-β-内啡肽阿片受体位点的丧失,但在SK - N - SH神经母细胞瘤细胞中则不会。

Rapid agonist-induced loss of 125I-beta-endorphin opioid receptor sites in NG108-15, but not SK-N-SH neuroblastoma cells.

作者信息

Cone R I, Lameh J, Sadée W

机构信息

School of Pharmacy, University of California, San Francisco 94143.

出版信息

Life Sci. 1991;49(19):PL147-52. doi: 10.1016/0024-3205(91)90396-s.

Abstract

We have measured mu and delta opioid receptor sites on intact SK-N-SH and NG108-15 neuroblastoma cells, respectively, in culture. Use of 125I-beta-endorphin (beta E) as a tracer, together with beta E(6-31) to block high-affinity non-opioid binding in both cell lines, permitted the measurement of cell surface mu and delta opioid receptor sites. Labeling was at delta sites in NG108-15 cells and predominantly at mu sites in SK-N-SH cells. Pretreatment with the mu and delta agonist, DADLE, caused a rapid loss of cell surface delta receptor sites in NG108-15 cells, but failed to reduce significantly mu receptor density in SK-N-SH cells.

摘要

我们分别测量了培养中的完整SK-N-SH和NG108-15神经母细胞瘤细胞上的μ和δ阿片受体位点。使用¹²⁵I-β-内啡肽(βE)作为示踪剂,并结合βE(6-31)来阻断两种细胞系中的高亲和力非阿片类结合,从而能够测量细胞表面的μ和δ阿片受体位点。在NG108-15细胞中标记位于δ位点,而在SK-N-SH细胞中主要位于μ位点。用μ和δ激动剂DADLE预处理导致NG108-15细胞中细胞表面δ受体位点迅速丧失,但未能显著降低SK-N-SH细胞中的μ受体密度。

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