Reggiani A, Carenzi A, Bella D D
Zambon Farmaceutici Research Laboratories, Bresso-Milan, Italy.
NIDA Res Monogr. 1986;75:347-50.
In the present paper a further evidence of a functional link between opioids and beta-receptor system in cultured rat C6 cells is presented. We showed that C6 cell exposure to Desmethylimipramine (DMI) causes expression of opioid receptors and loss of beta-receptors. We now show that C6 cells exposure to DMI causes an increase of intracellular levels of opioid peptides and an increase of aminopeptidase activity. In addition, the presence of the aminopeptidase inhibitor bestatin during cell exposure inhibits DMI-induced beta-receptor loss. These results indicate that cell exposure to DMI causes the full expression of the opioid peptide system. This effect could be related to changes of beta-receptor system.
在本论文中，提出了培养的大鼠C6细胞中阿片类物质与β受体系统之间功能联系的进一步证据。我们发现，C6细胞暴露于去甲丙咪嗪（DMI）会导致阿片受体表达以及β受体丧失。我们现在表明，C6细胞暴露于DMI会导致细胞内阿片肽水平升高以及氨肽酶活性增加。此外，细胞暴露期间氨肽酶抑制剂贝司他汀的存在会抑制DMI诱导的β受体丧失。这些结果表明，细胞暴露于DMI会导致阿片肽系统的充分表达。这种效应可能与β受体系统的变化有关。
