Eiring A, Manier D H, Bieck P R, Howells R D, Sulser F
Department of Psychiatry, Vanderbilt University School of Medicine, Nashville, TN 37232.
Brain Res Mol Brain Res. 1992 Dec;16(3-4):211-4. doi: 10.1016/0169-328x(92)90227-3.
C6 rat glioma cells were utilized as a model system to probe the 'serotonin/norepinephrine link' at the level of preproenkephalin (PPE) gene expression. The beta adrenoceptor mediated increase in PPE mRNA was attenuated by the selective beta 1 adrenoceptor antagonist metoprolol which blocked the isoproterenol induced cyclic AMP generation by 97%. The subtype nonspecific antagonist propranolol blocked both the isoproterenol induced increase in cyclic AMP and the increase in the PPE mRNA steady-state levels. Serotonin (5-HT) had no effect on the density of beta adrenoceptors or their down-regulation by isoproterenol and did not alter the PPE gene expression in the absence of the beta signal. However, 5-HT significantly deamplified the beta signal mediated enhancement of the PPE mRNA thus indicating that the aminergic link occurs beyond the beta adrenoceptor.
C6大鼠胶质瘤细胞被用作一个模型系统,以在脑啡肽原(PPE)基因表达水平上探究“血清素/去甲肾上腺素联系”。β肾上腺素能受体介导的PPE mRNA增加被选择性β1肾上腺素能受体拮抗剂美托洛尔减弱,美托洛尔使异丙肾上腺素诱导的环磷酸腺苷(cAMP)生成受阻97%。非亚型特异性拮抗剂普萘洛尔既阻断了异丙肾上腺素诱导的cAMP增加,也阻断了PPE mRNA稳态水平的增加。血清素(5-羟色胺,5-HT)对β肾上腺素能受体的密度或异丙肾上腺素对其的下调没有影响,并且在没有β信号的情况下不改变PPE基因表达。然而,5-HT显著减弱了β信号介导的PPE mRNA增强,因此表明胺能联系发生在β肾上腺素能受体之后。