Allouche S, Roussel M, Marie N, Jauzac P
Laboratory of Biochemistry A, University of Caen, C.H.U. Côte de Nacre, France.
Eur J Pharmacol. 1999 Apr 29;371(2-3):235-40. doi: 10.1016/s0014-2999(99)00180-6.
The efficacy of different opioid agonists to induce acute desensitization of the human delta-opioid receptor-mediated inhibition of cAMP accumulation was investigated in the neuroblastoma cell line SK-N-BE, which endogenously expresses these receptors. While etorphine, a non-selective alkaloid agonist, caused 50% desensitization after a 30-min incubation, the same treatment in the presence of the selective peptide agonists, DPDPE ([D-Pen2,D-Pen5]enkephalin) and deltorphin I (Tyr-D-Ala-Phe-Asp-Val-Val-Gly), almost totally desensitized the delta-opioid receptor-mediated inhibition of adenylyl cyclase. When SK-N-BE cells were prechallenged either with alkaloid or peptide agonist, we observed a cross-desensitization that was less marked when cells were pretreated with peptide agonists and then challenged with etorphine. Taken together, these results demonstrate that human delta-opioid receptors are differentially desensitized by alkaloid and peptide agonists.
在神经母细胞瘤细胞系SK-N-BE中研究了不同阿片样物质激动剂诱导人δ-阿片样物质受体介导的环磷酸腺苷（cAMP）积累抑制急性脱敏的功效，该细胞系内源性表达这些受体。非选择性生物碱激动剂埃托啡在孵育30分钟后可引起50%的脱敏，而在选择性肽激动剂DPDPE（[D-青霉胺2，D-青霉胺5]脑啡肽）和强啡肽I（酪氨酸-D-丙氨酸-苯丙氨酸-天冬氨酸-缬氨酸-缬氨酸-甘氨酸）存在的情况下进行相同处理，几乎可使δ-阿片样物质受体介导的腺苷酸环化酶抑制完全脱敏。当SK-N-BE细胞先用生物碱或肽激动剂进行预激发时，我们观察到一种交叉脱敏现象，当细胞先用肽激动剂预处理然后用埃托啡激发时，这种交叉脱敏现象不太明显。综上所述，这些结果表明人δ-阿片样物质受体对生物碱和肽激动剂的脱敏作用存在差异。
