长期暴露于百日咳毒素会改变神经母细胞瘤x胶质瘤NG108-15杂交细胞中由毒蕈碱受体介导的环磷酸腺苷代谢调节。

Chronic exposure to pertussis toxin alters muscarinic receptor-mediated regulation of cyclic AMP metabolism in neuroblastoma x glioma NG108-15 hybrid cells.

作者信息

Westlind-Danielsson A, Gillenius P, Askelöf P, Bartfai T

机构信息

Department of Biochemistry, University of Stockholm, Sweden.

出版信息

J Neurochem. 1988 Jul;51(1):38-44. doi: 10.1111/j.1471-4159.1988.tb04832.x.

DOI:10.1111/j.1471-4159.1988.tb04832.x

PMID:2454296

Abstract

Chronic pertussis toxin treatment (5 days) of NG108-15 neuroblastoma X glioma hybrid cells had no significant effect on basal cyclic AMP levels whereas it effectively blocked the inhibitory action of acute (10 min) exposure of carbachol (10(-4)M) on intracellular cyclic AMP accumulation, stimulated by prostaglandin E1. This action of pertussis toxin was found to be long lasting: exposure of the cells to pertussis toxin (100 ng/ml) for only 24 h followed by a 5-day withdrawal period still was shown effective on day 7 in abolishing the inhibitory action of carbachol on prostaglandin E1-stimulated cyclic AMP production. Chronic exposure (5 days) of NG108-15 cells to carbachol (10(-5)M) causes an increase in basal cyclic AMP levels by 98%, and a desensitization of the muscarinic inhibition of cyclic AMP accumulation, assessed after a 24-h withdrawal period. When carbachol treatment is carried out in the presence of pertussis toxin (100 ng/ml) both of these effects of carbachol are abolished.

摘要

用百日咳毒素对NG108 - 15神经母细胞瘤X胶质瘤杂交细胞进行慢性处理（5天），对基础环磷酸腺苷（cAMP）水平没有显著影响，然而它有效地阻断了卡巴胆碱（10⁻⁴M）急性（10分钟）暴露对前列腺素E1刺激的细胞内环磷酸腺苷积累的抑制作用。发现百日咳毒素的这种作用具有持久性：细胞仅暴露于百日咳毒素（100 ng/ml）24小时，随后经过5天的撤药期，在第7天仍显示出对卡巴胆碱抑制前列腺素E1刺激的环磷酸腺苷产生的作用有效。将NG108 - 15细胞慢性暴露（5天）于卡巴胆碱（10⁻⁵M）会使基础环磷酸腺苷水平增加98%，并且在24小时撤药期后评估，会使环磷酸腺苷积累的毒蕈碱抑制作用脱敏。当在百日咳毒素（100 ng/ml）存在的情况下进行卡巴胆碱处理时，卡巴胆碱的这两种作用都被消除。